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1.AA Caspase-9 is an initiator caspase, encoded by the CASP9 gene.

The aspartic acid specific protease caspase-9 has been linked to the mitochondrial death pathway. t is acti!ated d"ring programmed cell death #apoptosis$. nd"ction of stress signaling pathways %&'(SAP' ca"ses release of cytochrome c from mitochondria and acti!ation of apaf1 #apoptosome$, which in t"rn clea!es the pro-en)yme of caspase-9 into the acti!e form. *.AA Primary symptoms of C. par!"m infection are ac"te, watery, and non-bloody diarrhoea. C. par!"m infection is of partic"lar concern in imm"nocompromised patients, where diarrhea can reach 1+,1-. per day. /ther symptoms may incl"de anore0ia, na"sea(!omiting and abdominal pain. nfection is ca"sed by ingestion of spor"lated oocysts transmitted by the fecal-oral ro"te 1ntamoeba histolytica is an anaerobic parasitic proto)oan.The acti!e #tropho)oite$ stage e0ists only in the host and in fresh loose feces2 cysts s"r!i!e o"tside the host in water, in soils, and on foods, especially "nder moist conditions on the latter. http3(("pload.wikimedia.org(wikipedia(commons(c(cf(Tropho)oites4of41ntamoeba4...rocytes.%P 5 http3((en.wikipedia.org(wiki(6ile31ntamoeba4histolytica4life4cycle-en.s!g 5iardia lamblia is a flagellated proto)oan parasite that coloni)es and reprod"ces in the small intestine, ca"sing giardiasis. The giardia parasite attaches to the epitheli"m by a !entral adhesi!e disc, and reprod"ces !ia binary fission. 5iardiasis does not spread !ia the bloodstream, nor does it spread to other parts of the gastro-intestinal tract, b"t remains confined to the l"men of the small intestine. http3(("pload.wikimedia.org(wikipedia(commons(+(+7(5iardia4lamblia4S184799...74lores.:pg 5iardia infection can occ"r thro"gh ingestion of dormant cysts in contaminated water, food, or by the faecal-oral ro"te #thro"gh poor hygiene practices$. The 5iardia cyst can s"r!i!e for weeks to months in cold water, and therefore can be present in contaminated wells and water systems, especially stagnant water so"rces s"ch as nat"rally occ"rring ponds, storm water storage systems, and e!en clean-looking mo"ntain streams. http3((en.wikipedia.org(wiki(6ile35iardia4life4cycle4en.s!g Strongyloides stercoralis is a nematode that can parasiti)e h"mans. The ad"lt parasitic stage li!es in t"nnels in the m"cosa of the small intestine.Strongyloides stercoralis is a nematode that

can parasiti)e h"mans. The ad"lt parasitic stage li!es in t"nnels in the m"cosa of the small intestine. 8any people infected are "s"ally asymptomatic at first. Symptoms incl"de dermatitis3 swelling, itching, lar!a c"rrens, and mild hemorrhage at the site where the skin has been penetrated. f the parasite reaches the l"ngs, the chest may feel as if it is b"rning, and whee)ing and co"ghing may res"lt, along with pne"monia-like symptoms #.;ffler<s syndrome$. 1!ent"ally, the intestines co"ld be in!aded, leading to b"rning pain, tiss"e damage, sepsis, and "lcers. n se!ere cases, edema may res"lt in obstr"ction of the intestinal tract as well as loss of peristaltic contractions. Strongyloidiasis in imm"nocompetent indi!id"als is "s"ally an indolent disease. =owe!er, in imm"nocompromised indi!id"als, strongyloidiasis can ca"se a hyperinfecti!e syndrome #also called disseminated strongyloidiasis$ d"e to the reprod"cti!e capacity of the parasite inside the host. This hyperinfecti!e syndrome has a mortality rate of close to 9+>. http3((en.wikipedia.org(wiki(6ile3Strongyloides4stercorali)4lar!a.:pg ?.@ A* microglob"lin is a component of 8=C class molec"les, which are present on all n"cleated cells #e0cl"des red blood cells$.8ice models deficient for the A* microglob"lin gene ha!e been engineered. These mice demonstrate that A* microglob"lin is necessary for cell s"rface e0pression of 8=C class and stability of the peptide binding groo!e. n fact, in the absence of A* microglob"lin, !ery limited amo"nts of 8=C class #classical and non-classical$ molec"les can be detected on the s"rface. n the absence of 8=C class , CB7 T cells cannot de!elop. #CB7 T cells are a s"bset of T cells in!ol!ed in the de!elopment of acC"ired imm"nity.$.ow le!els of A* microglob"lin can indicate non-progression of = D. .e!els of beta-* microglob"lin can be ele!ated in m"ltiple myeloma and lymphoma,tho"gh in these cases primary amyloidosis #amyloid light chain$ and secondary amyloidosis #Amyloid associated protein$ are more common

E.@@ Calcitriol , also called 1,*--dihydro0ycholecalciferol or 1,*--dihydro0y!itamin B?, is the hormonally acti!e form of !itamin B with three hydro0yl gro"ps. t increases the le!el of calci"m #Ca*F$ in the blood by #1$ increasing the "ptake of calci"m from the g"t into the blood, #*$ decreasing the transfer of calci"m from blood to the "rine by the kidney, and #?$ increasing the release of calci"m into the blood from bone.

Calcitriol is prod"ced in the cells of the pro0imal t"b"le of the nephron in the kidneys by the action of *--hydro0y!itamin B? 1-alpha-hydro0ylase

-.11 consistent "se of CS6-PCG for =SD serology established a diagnosis in the ma:ority of ac"te aseptic meningitis patients.

9.CC

1sophageal !arices are e0tremely dilated s"b-m"cosal !eins in the lower esophag"s. They are most often a conseC"ence of portal hypertension, commonly d"e to cirrhosis2 patients with esophageal !arices ha!e a strong tendency to de!elop bleeding.

The ma:ority of blood from the esophag"s is drained !ia the esophageal !eins, which carry deo0ygenated blood from the esophag"s to the a)ygos !ein, which in t"rn drains directly into the s"perior !ena ca!a. These !eins ha!e no part in the de!elopment of esophageal !arices.

The remaining blood from the esophag"s is drained into the s"perficial !eins lining the esophageal m"cosa, which drain into the coronary !ein #left gastric !ein$, which in t"rn drains directly into the portal !ein. These s"perficial !eins #normally only appro0imately 1mm in diameter$ become distended "p to 1,* cm in diameter in association with portal hypertension.

http3(("pload.wikimedia.org(wikipedia(commons(b(b9(1sophageal4!arices...4-4wale.:pg H.11 B C leads to the formation of small blood clots inside the blood !essels thro"gho"t the body. As the small clots cons"me coag"lation proteins and platelets, normal coag"lation is disr"pted and abnormal bleeding occ"rs from the skin #e.g. from sites where blood samples were taken$, the gastrointestinal tract, the respiratory tract and s"rgical wo"nds. The small clots also disr"pt normal blood flow to organs #s"ch as the kidneys$, which may malf"nction as a res"lt. The acti!ation of the coag"lation cascade yields thrombin that con!erts fibrinogen to fibrin2 the stable fibrin clot being the final prod"ct of hemostasis. The fibrinolytic system then f"nctions to break down fibrinogen and fibrin. Acti!ation of the fibrinolytic system generates plasmin #in the presence of thrombin$, which is responsible for the lysis of fibrin clots. The breakdown of fibrinogen and fibrin res"lts in polypeptides called fibrin degradation prod"cts #6BPs$ or fibrin split prod"cts #6SPs$. n a state of homeostasis, the presence of plasmin is critical, as it is the central proteolytic en)yme of coag"lation and is also necessary for the breakdown of clots, or

fibrinolysis. 7.@@ p-? is a t"mor s"ppressor protein that in h"mans is encoded by the TP-? gene. p-? is important in m"lticell"lar organisms, where it reg"lates the cell cycle and, th"s, f"nctions as a t"mor s"ppressor that is in!ol!ed in pre!enting cancer p-? has many mechanisms of anticancer f"nction, and plays a role in apoptosis, genomic stability, and inhibition of angiogenesis. n its anti-cancer role, p-? works thro"gh se!eral mechanisms3 t can acti!ate B&A repair proteins when B&A has s"stained damage. t can ind"ce growth arrest by holding the cell cycle at the 51(S reg"lation point on B&A damage recognition #if it holds the cell here for long eno"gh, the B&A repair proteins will ha!e time to fi0 the damage and the cell will be allowed to contin"e the cell cycle$. t can initiate apoptosis, the programmed cell death, if B&A damage pro!es to be irreparable.

f the TP-? gene is damaged, t"mor s"ppression is se!erely red"ced. People who inherit only one f"nctional copy of the TP-? gene will most likely de!elop t"mors in early ad"lthood, a disease known as .i-6ra"meni syndrome. The TP-? gene can also be damaged in cells by m"tagens #chemicals, radiation, or !ir"ses$, increasing the likelihood that the cell will begin decontrolled di!ision. 8ore than -+ percent of h"man t"mors contain a m"tation or deletion

9. A The renin-angiotensin system #GAS$ or the renin-angiotensin-aldosterone system #GAAS$ is a hormone system that reg"lates blood press"re and water #fl"id$ balance. Ihen blood !ol"me is low, :"0taglomer"lar cells in the kidneys secrete renin. Genin stim"lates the prod"ction of angiotensin , which is then con!erted to angiotensin . Angiotensin ca"ses blood !essels to constrict, res"lting in increased blood press"re. Angiotensin also stim"lates the secretion of the hormone aldosterone from the adrenal corte0. Aldosterone ca"ses the t"b"les of the kidneys to increase the reabsorption of sodi"m and water into the blood. This increases the !ol"me of fl"id in the body, which also increases blood press"re. f the renin-angiotensin-aldosterone system is too acti!e, blood press"re will be too high. There are many dr"gs that interr"pt different steps in this system to lower blood press"re. These dr"gs are one of the main ways to control high blood press"re #hypertension$, heart fail"re, kidney fail"re, and harmf"l effects of diabetes.J*KJ? Acti!ation

The system can be acti!ated when there is a loss of blood !ol"me or a drop in blood press"re #s"ch as in hemorrhage$. Alternati!ely, a decrease in plasma &aCl concentration will stim"late the mac"la densa to release renin. 1. f the perf"sion of the :"0taglomer"lar apparat"s in the kidney<s mac"la densa decreases, then the :"0taglomer"lar cells release the en)yme renin. *. Genin clea!es a )ymogen, an inacti!e peptide, called angiotensinogen, con!erting it into angiotensin . ?. Angiotensin is then con!erted to angiotensin by angiotensin-con!erting en)yme #AC1$JEK which was tho"ght to be fo"nd mainly in l"ng capillaries. =owe!er new e!idence s"ggests the AC1 is fo"nd in all blood !essel endothelial cells.J-K E. Angiotensin is the ma:or bioacti!e prod"ct of the renin-angiotensin system, binding to receptors on intraglomer"lar mesangial cells, ca"sing these cells to contract along with the blood !essels s"rro"nding them and ca"sing the release of aldosterone from the )ona glomer"losa in the adrenal corte0. Angiotensin acts as an endocrine, a"tocrine(paracrine, and intracrine hormone. http3((en.wikipedia.org(wiki(Genin-angiotensin4system 9.AA

Ihen blood !ol"me is low, :"0taglomer"lar cells in the kidneys secrete renin. Genin stim"lates the prod"ction of angiotensin , which is then con!erted to angiotensin . Angiotensin ca"ses blood !essels to constrict, res"lting in increased blood press"re. Angiotensin also stim"lates the secretion of the hormone aldosterone from the adrenal corte0. Aldosterone ca"ses the t"b"les of the kidneys to increase the reabsorption of sodi"m and water into the blood. This increases the !ol"me of fl"id in the body, which also increases blood press"re. so when blood !ol"m is become higher by recei!ing 1 liter fl"id........Ldec. renin-angiotensin aldosteron system 1+.11 /steopetrosis,, also known as marble bone disease is an e0tremely rare inherited disorder whereby the bones harden, becoming denser,&ormal bone growth is achie!ed by a balance between bone formation by osteoblasts and bone resorption #break down of bone matri0$ by osteoclasts. n osteopetrosis, the n"mber of osteoclasts may be red"ced, normal, or increased. 8ost importantly, osteoclast dysf"nction mediates the pathogenesis of this disease. deficiency of carbonic anhydrase in osteoclasts is noted. The absence of this en)yme ca"ses defecti!e hydrogen ion p"mping by osteoclasts and this in t"rn ca"ses defecti!e bone resorption by osteoclasts, as an acidic en!ironment is needed for dissociation of calci"m hydro0yapatite from bone matri0. =ence, bone resorption fails while its formation persists.

10cessi!e bone is formed. /steopetrosis 3 Calci"m...."naffected Phosphate..."naffected Alkalin phosphatase....ele!ated Parathyroid =ormone...."naffected

Symptoms3Pain 6reC"ent fract"res, especially of the long bones, which often do not heal &er!e compression, leading to headache, blindness, deafness =ematological diffic"lties, incl"ding anemic thrombocytopenia, le"kopenia 1nlarged spleen /steomyelitis 6rontal bossing of the sk"ll Mn"s"al dentition, incl"ding malformed and "nerr"pted teeth nfection @leeding Stroke 11. B Gespiratory Acidosis3 Ph N, P/* N, PC/* O, represented by the letters P - I 11.B Phenobarbital ca"ses a QdepressionQ of the body<s systems, mainly the central and peripheral ner!o"s systems2 th"s, the main characteristic of phenobarbital o!erdose is a QslowingQ of bodily f"nctions, incl"ding decreased conscio"sness #e!en coma$, bradycardia, bradypnea, hypothermia, and hypotension #in massi!e o!erdoses$. /!erdose may also lead to p"lmonary edema and ac"te renal fail"re as a res"lt of shock. decreased respiration #hypo!entilation$ ca"ses increased blood carbon dio0ide and decreased o* and p= #a condition generally called acidosis$.

RRRRRRRRRRRRRRRCorrectionRRRRRRRRRRRRRRR Ss 11 RRRRRRRRRRRRRRRRRRRRRRRRR @arbit"rate o!erdose Poisoning by barbit"rates Classification and e0ternal reso"rces CB-1+ TE*.? e8edicine med(*+H Phenobarbital ca"ses a QdepressionQ of the body<s systems, mainly the central and peripheral ner!o"s systems2 th"s, the main characteristic of phenobarbital o!erdose is a QslowingQ of bodily f"nctions, incl"ding decreased conscio"sness #e!en coma$, bradycardia, bradypnea, hypothermia, and hypotension #in massi!e o!erdoses$. /!erdose may also lead to p"lmonary edema and ac"te renal fail"re as a res"lt of shock.

The electroencephalogram of a person with phenobarbital o!erdose may show a marked decrease in electrical acti!ity, to the point of mimicking brain death. This is d"e to profo"nd depression of the central ner!o"s system, and is "s"ally re!ersible.J*EK 1*. B 8a:or Bepressi!e Bisorder3 Characteri)ed by at least - of the following 9 symptoms for * weeks. Symptoms m"st incl"de patient - report depressed mood or anhedonia3 1. Sleep dist"rbance *. loss of interest # anhedonia$ ?. 5"ilt or feeling of worthlessness E. .oss of energy -. .oss of concentration 9. Appetite( weight changes H. Psychomotor retardation or agitation 7. S"icidal ideations 9. Bepressed mood #6A page EE?$

1?. B 'ey answer is B and wo"ld go for B too. 1?. B G"le T9- &egociate3 &egotiate rather than order a. Treatment choices are the res"lt of agreement, noy commands by the physician. c. Gelationship and agreement s"pport adherence. #'aplan @S book page 1?1$

G"le T 19- Accept the health beliefs of the patients a. @e accepting of benign folk medicine practice. 10pect them. B0 need to be e0plained in the way patients can "nderstand, e!en if not technically precise. b. /ffer to e0plain things to family members for the patients. #'aplan @S book page 1??$

1?. @ 5o"t3 Asymetric :oint distrib"tion. %oint is swollen, red, and painf"l. classic manifestation is painf"ll 8TP :oint of the big toe # Podagra$. Toph"s formation often on e0ternal ear, oleocranon b"rsa, or achiles tendon. Ac"te attack tends to occ"r after a large meal or alcohol cons"mption # alcohol metabolism compete for same e0cretion sites in the kidney as "ric acid, ca"sing decrease "ric acid secretion and s"bseC"ent b"ild"p in blood. 6indidng3 Precipitation of monosodic "reate crystals into :oints d"e to hyper"ricemia, which can be ca"sed by .esch &yhan Syndrome, PGPP e0cess.... Crystals are needle shaped birefringentU yellow "nder parallel light TT/3 Colchicine, &SA Bs, probenecid, allop"rinol. 6A page ?7+ RRRRRRRRRRRRRRRRRRCorretion RRRRRRRRRRRRRRRR 1E. @ 5o"t3 Asymetric :oint distrib"tion. %oint is swollen, red, and painf"l. classic manifestation is painf"ll 8TP :oint of the big toe # Podagra$. Toph"s formation often on e0ternal ear, oleocranon b"rsa, or achiles tendon. Ac"te attack tends to occ"r after a large meal or alcohol cons"mption # alcohol metabolism compete for same e0cretion sites in the kidney as "ric acid, ca"sing decrease "ric acid secretion and s"bseC"ent b"ild"p in blood. 6indidng3 Precipitation of monosodic "reate crystals into :oints d"e to hyper"ricemia, which can be ca"sed by .esch &yhan Syndrome, PGPP e0cess....

Crystals are needle shaped birefringentU yellow "nder parallel light TT/3 Colchicine, &SA Bs, probenecid, allop"rinol. 6A page ?7+

1-.AA 1-=emoglobin is an assembly of fo"r glob"lar protein s"b"nits#polypeptide chains$.... *- 1ach s"b"nit is composed of a protein chain tightly associated with a non-protein heme gro"p. ?-1ach protein chain arranges into a set of alpha-heli0 str"ct"ral segments connected together in a globin fold arrangement, E.Ad"lt hemoglobin is made of * alpha and * beta chains --These fo"r polypeptide chains are bo"nd to each other and stabili)ed by a- salt bridges...which is a nonco!alent bonding...d"e to interaction between anionic carbo0ylate #GC//-$ and cationic ammoni"m #G&=?F$ in the amino acids b-hydrogen bonds, c- hydrophobic interactions....oil and water donot combine bec"ase of hydrophobic interaction ...and hydrophobic interaction is a property of nonpolar molec"les and this interaction is also "sed in the case of protein folding where by most folded proteins ha!e a hydrophobic core in which side chain packing stabili)es the folded state, and charged or polar side chains on the sol!ent-e0posed s"rface where they interact with s"rro"nding water molec"les. 9-the hydrophobic effect is important to "nderstand the str"ct"re of proteins that ha!e hydrophobic amino acids, s"ch as alanine, !aline, le"cine, isole"cine, phenylalanine, and methionine gro"ped together with the protein...and hydrophobic interaction is between indi!id"al aminoacids H-/rdinarily, the hemoglobin molec"les e0ist as single, isolated "nits in the red cell, whether they ha!e o0ygen bo"nd or not... 7-Sickle hemoglobin e0ists as isolated "nits in the red cells when they ha!e o0ygen bo"nd. 9-Ihen sickle hemoglobin releases o0ygen in the peripheral tiss"es, howe!er, the molec"les tend to stick together and form long chains or polymers

.et "s see what happens in sickle cell anemia...gl"tamic acid#hydrophillic $ is replaced by hydrophobic !aline #which increases the n"mber of hydrophobic aminoacids ...which int"rn

increases hydrophobic interactions $ ..and these hydrophobic interactions stabili)e the polymeri)ed sickle hemoglobin....

19.B Significant f"nctional aspects of the occipital lobe is that it contains the primary !is"al corte0 and is the part of the brain where dreams come from. A. Ca"date n"cle"s @. Primary motor corte0 area C. Thalam"s 1. Posterior .imb 19.B =omonymo"s hemianopsia can be congenital, b"t is "s"ally ca"sed by brain in:"ry s"ch as from stroke, tra"ma, t"mors, infection, or following s"rgery. Dasc"lar and neoplastic #malignant or benign t"mo"rs$ lesions from the optic tract, to !is"al corte0 can ca"se a contralateral homonymo"s hemianopsia. n:"ry to the right side of the brain will affect the left !is"al fields of each eye. The more posterior the cerebral lesion, the more symmetric #congr"o"s$ the homonymo"s hemianopsia will be. 6or e0ample, a person who has a lesion of the right optic tract will no longer see ob:ects on his left side. Similarly, a person who has a stroke to the right occipital lobe will ha!e the same !is"al field defect, "s"ally more congr"ent between the two eyes, and there may be mac"lar sparing. A stroke on the right side of the brain #especially parietal lobe$, in addition to prod"cing a homonymo"s hemianopsia, may also lead to the syndrome of hemispatial neglect. 1H.1 Schi)oid personality disorder #SPB$ is a personality disorder characteri)ed by a lack of interest in social relationships, sometimes se0"ally apathetic, a tendency towards a solitary lifestyle, secreti!eness, and emotional coldness. SPB is not the same as schi)ophrenia, altho"gh they share some similar characteristics s"ch as detachment or bl"nted affect and there is increased pre!alence of the disorder in families with schi)ophrenia. 17. C 5ardner syndrome, also known as familial colorectal polyposis, is an a"tosomal dominant form of polyposis characteri)ed by the presence of m"ltiple polyps in the colon together with t"mors o"tside the colon.The e0tracolonic t"mors may incl"de osteomas of the sk"ll, thyroid cancer, epidermoid cysts, fibromas and sebaceo"s cysts, as well as the occ"rrence of desmoid t"mors

in appro0imately 1-> of affected indi!id"als. The co"ntless polyps in the colon predispose to the de!elopment of colon cancer2 if the colon is not remo!ed, the chance of colon cancer is considered to be !ery significant. Polyps may also grow in the stomach, d"oden"m, spleen, kidneys, li!er, mesentery and small bowel. n a small n"mber of cases, polyps ha!e also appeared in the cerebell"m. Cancers related to 5S commonly appear in the thyroid, li!er and kidneys. At this time, there is no c"re, and in its more ad!anced forms, it is considered a terminal diagnosis with a life e0pectancy of ?-,E- years2 treatments are s"rgery and palliati!e care, altho"gh some chemotherapy has been tried with limited s"ccess. 5ardner syndrome is now known to be ca"sed by m"tation in the APC gene located in chromosome -C*1 #band C*1 on chromosome -$. This is the same gene as is m"tant in familial adenomato"s polyposis #6AP$, a more common disease that also predisposes to colon cancer. 19.1 The "terine artery "s"ally arises from the anterior di!ision of the internal iliac artery. t tra!els to the "ter"s, crossing the "reter anteriorly, reaching the "ter"s by tra!eling in the cardinal ligament. t tra!els thro"gh the parametri"m of the inferior broad ligament of the "ter"s. t commonly anastomoses #connects with$ the o!arian artery. The "terine artery is the ma:or blood s"pply to the "ter"s and enlarges significantly d"ring pregnancy.

*+.B Transitional cell carcinoma #TCC, also "rothelial cell carcinoma or MCC$ is a type of cancer that typically occ"rs in the "rinary system3 the kidney, "rinary bladder, and accessory organs. t is the most common type of bladder cancer and cancer of the "reter, "rethra, and "rach"s2 it is the second most common type of kidney cancer. TCC arises from the transitional epitheli"m, a tiss"e lining the inner s"rface of these hollow organs. TCCs are often m"ltifocal, with ?+-E+> of patients ha!ing more than one t"mo"r at diagnosis. The pattern of growth of TCCs can be papillary, sessile #flat$ or carcinoma-in-sit" #C S$. The most common site of TCC metastasis o"tside the pel!is is bone #?->$2 of these bone metastases, E+> are in the spine. Ihen the term Q"rothelialQ is "sed, it specifically refers to a carcinoma of the "rotheli"m, meaning a TCC of the "rinary system.

http3((en.wikipedia.org(wiki(6ile3@ladder4"rothelial4carcinoma4#1$4pT1.%P5 http3((en.wikipedia.org(wiki(6ile3@lasent"mor.:pg

*1. @ 6actitio"s =ypoglycemia #self in:ection of ins"lin$. 5l"cose .. dec. ins"lin .. nc C peptide ... dec &o ketoacidosis.

C. P. ser!es as an important linker between the A- and the @- chains of ins"lin and facilitates the efficient assembly, folding, and processing of ins"lin in the endoplasmic retic"l"m. 1C"imolar amo"nts of C-peptide and ins"lin are then stored in secretory gran"les of the pancreatic beta cells and both are e!ent"ally released to the portal circ"lation. nitially, the sole interest in Cpeptide was as a marker of ins"lin secretion and has as s"ch been of great !al"e in f"rthering the "nderstanding of the pathophysiology of type 1 and type * diabetes. B"ring the past decade, howe!er, C-peptide has been fo"nd to be a bioacti!e peptide in its own right, with effects on micro!asc"lar blood flow and tiss"e health. C-peptide sho"ld not be conf"sed with c-reacti!e protein or Protein C. &ewly diagnosed diabetes patients often get their C-peptide le!els meas"red as a means of disting"ishing type 1 diabetes and type * diabetes. C-peptide le!els are meas"red instead of ins"lin le!els beca"se ins"lin concentration in the portal !ein ranges from two to ten times higher than in the peripheral circ"lation. The li!er e0tracts abo"t half the ins"lin reaching it in the plasma, b"t this !aries with the n"tritional state. The pancreas of patients with type 1 diabetes is "nable to prod"ce ins"lin and therefore they will "s"ally ha!e a decreased le!el of C-peptide, whereas C-peptide le!els in type * patients are normal or higher than normal. 8eas"ring Cpeptide in patients in:ecting synthetic ins"lin can help to determine how m"ch of their own nat"ral ins"lin these patients are still prod"cing, of if they prod"ce any at all. C-peptide is also "sed for determining the possibility of gastrinomas associated with 8"ltiple 1ndocrine &eoplasm syndromes #81& 1$. Since a significant n"mber of gastrinomas are associated with 81& in!ol!ing other hormone prod"cing organs #pancreas, parathyroids, and pit"itary$, higher le!els of C-peptide together with the presence of a gastrinoma s"ggest that organs besides the stomach may harbor neoplasms. C-peptide le!els are checked in women with Polycystic /!arian Syndrome #PC/S$ to determine

degree of ins"lin resistance. @oth e0cess body weight and a high plasma concentration of C-peptide predispose men with a s"bseC"ent diagnosis of prostate cancer to an increased likelihood of dying of the disease, according to the res"lts of a long-term s"r!i!al analysis reported in the /ctober 9, *++7

**.@@ ....the patient is e0posed to high le!els of radiation and this ca"ses ac"te radiation syndrome Stages of Ac"te radiation Syndrome 1$ prodrome...na"sea, !omiting, anore0ia, fatig"e, diarrhea, abdominal cramping, and dehydration which are 5 T Symptom *$ clinical latency, ?$ manifest illness, and E$ reco!ery or death my answer is 5 T here is the link http3((emedicine.medscape.com(article(7?E+1--o!er!iew

*?.BB

The pit"itary stalk #also known as the inf"ndib"lar stalk or simply the inf"ndib"l"m$ is the connection between the hypothalam"s and the posterior pit"itary. t carries a0ons from the magnocell"lar ne"rosecretory cells of the hypothalam"s down to the posterior pit"itary where they release their hormones into the blood.This connection is called the hypothalamohypophyseal tract, and is responsible for the release of o0ytocin and antidi"retic hormone......All choices e0cept /0ytocin are hormones of anterior pit"itary

*E.BB n the C"estion we are asked abo"t heterogeneity#!ariability$ -The distances between the scores and the mean #Vi-8$ are called de!iations -The greater the !ariety or heterogeneity of the scores, the greater the de!iations - f the scores were cl"stered aro"nd the mean, the de!iations wo"ld be small, b"t they wo"ld

increase as the scores became more spread o"t or more !aried. -And one way to meas"re !ariability #heterogeno"s pop"lation in this case $ is by calc"lating the !al"e of the Standard Be!iation .. -5enerally SB - is an inde0 of !ariability3 the SB increases in !al"e as the distrib"tion becomes more !ariable. The less the !ariability in the distrib"tion, the lower the !al"e of the SB. n short when we get high SB that means high !ariabilty #high heterogeno"s pop"lation in this case$....low SB means low !ariabilty #less hetrogeno"s pop"lation $...So to check !ariabilty#hterogeneity$ ...compare the standard de!iation !al"es not the mean of the e0periment... *-.@@

.ight in either retina sends a signal !ia C& to pretectal n"clei in 8 B@GA & that acti!ate bilateral 1B &51G-I1STP=A. n"clei2p"pil contract bilateraly Cranial ner!e n"clei3 C& , D......8idbrain

....D,D ,D ,D ...Pons .... V,V,V ,V ....8ed"lla *9.AA

Co0sackie!ir"s is a !ir"s that belongs to a family of non en!eloped linear positi!e-sense ssG&A !ir"ses, Picorna!iridae and the gen"s 1ntero!ir"s, which also incl"des polio!ir"s and echo!ir"s.5ro"p A co0sackie!ir"ses tend to infect the skin and m"co"s membranes, ca"sing herpangina, ac"te hemorrhagic con:"ncti!itis #A=C$, and hand, foot and mo"th #=68$ disease. @oth gro"p A and gro"p @ co0sackie!ir"ses can ca"se nonspecific febrile illnesses, rashes, "pper respiratory tract disease, and aseptic meningitis.5ro"p @ co0sackie!ir"ses tend to infect the heart, ple"ra, pancreas, and li!er, ca"sing ple"rodynia, myocarditis, pericarditis, and hepatitis #inflammation of the li!er not related to the hepatotropic !ir"ses$Co0sackie @ infection of the heart can lead to pericardial eff"sion. 8"ffled heart so"nds and p"ls"s parado0"s are signs of this.

*H.BB

8oll"sc"m contagios"m #8C$ is a !iral infection of the skin or occasionally of the m"co"s membranes. t is ca"sed by a B&A po0!ir"s called the moll"sc"m contagios"m !ir"s #8CD$. 8CD has no animal reser!oir, infecting only h"mans.The !ir"s commonly spreads thro"gh skinto-skin contact. This incl"des se0"al contact or to"ching or scratching the b"mps and then to"ching the skin. =andling ob:ects that ha!e the !ir"s on them #fomites$, s"ch as a towel, can also res"lt in infection.8oll"sc"m contagios"m is contagio"s "ntil the b"mps are gone-which, if "ntreated, may be "p to 9 months or longer.8oll"sc"m contagios"m lesions are flesh-colored, dome-shaped, and pearly in appearance. They are often 1,- millimeters in diameter, with a dimpled center. They are generally not painf"l, b"t they may itch or become irritated. Picking or scratching the b"mps may lead to f"rther infection or scarring.

*7.11

@GCA1 is a h"man t"mor s"ppressor gene that prod"ces a protein called breast cancer type 1 s"sceptibility protein.@GCA1 is e0pressed in the cells of breast and other tiss"e, where it helps repair damaged B&A, or destroy cells if B&A cannot be repaired. f @GCA1 itself is damaged, damaged B&A is not repaired properly and this increases risks for cancers. Certain !ariations of the @GCA1 gene lead to an increased risk for breast cancer.Iomen with an abnormal @GCA1 or @GCA* gene ha!e "p to an 9+> risk of de!eloping breast cancer by age 9+2 increased risk of de!eloping o!arian cancer is abo"t --> for women with @GCA1 m"tations and abo"t *-> for women with @GCA* m"tations.

*9.BBDestib"locochlear ner!e....D ....hearing and balance

?+.CC The d"mping syndrome is 8ost people are "nable to tolerate certain foods after gastric bypass, especially foods with high s"gar or fat content. 1ating these foods can ca"se the Wd"mping syndrome,X which may ca"se nasea and !omiting, diarrhea, a bloated feeling, di))iness and sweating.

?1.B Ac"te intermittent porphyria #A P$ is a rare a"tosomal dominant. Mnder normal circ"mstances, heme synthesis begins in the mitochondrion, proceeds into the cytoplasm, and finishes back in the mitochondrion. =owe!er, witho"t porphobilinogen

deaminase, a necessary cytoplasmic en)yme, heme synthesis cannot finish, and the metabolite porphobilinogen acc"m"lates in the cytoplasm. Additional factors m"st also be present s"ch as hormones, dr"gs, and dietary changes that trigger the appearance of symptoms. Symptoms of A P may incl"de abdominal pain, constipation, and m"scle weakness. Patients with A P are commonly misdiagnosed with psychiatric diseases. S"bseC"ent treatment with anti-psychotics increases the acc"m"lation of porphrobiliogen, th"s aggra!ating the disease eno"gh that it may pro!e fatal.

?*.B @ot"lin"m to0in is a protein prod"ced by the bacteri"m Clostridi"m bot"lin"m, and is e0tremely ne"roto0ic The hea!y chain of the to0in is partic"larly important for targeting the to0in to specific types of a0on terminals. The to0in m"st get inside the a0on terminals in order to ca"se paralysis. 6ollowing the attachment of the to0in hea!y chain to proteins on the s"rface of a0on terminals, the to0in can be taken into ne"rons by endocytosis. The light chain is able to clea!e endocytotic !esicles and reach the cytoplasm. The light chain of the to0in has protease acti!ity. The type A to0in proteolytically degrades the S&AP-*- protein, a type of S&AG1 protein. The S&AP-*protein is reC"ired for !esicle f"sion that releases ne"rotransmitters from the a0on endings #in partic"lar Acetylcholine$.J-7K @ot"lin"m to0in specifically clea!es these S&AG1s, and so pre!ents ne"ro-secretory !esicles from docking(f"sing with the ner!e synapse plasma membrane and releasing their ne"rotransmitters.

?1.BB ACMT1 &T1G8 TT1&T P/GP=PG A......BM1 T/ MG/P/GP=PG &/51& SP&T=AS1 deficiency .....ca"ses acc"m"lation of porphobilinogen and delta -A.A in "rine symptoms...- P Painf"l abdomen pink "rine polyne"ropathy psychological dist"rbances precipitated by dr"g

Porphobilinogen #P@5$ is in!ol!ed in porphyrin metabolism. t is generated by aminole!"linate #A.A$ and the en)yme A.A dehydratase#is degenerated by .ead poisoning$. P@5 is then con!erted into hydro0ymethyl bilane by the en)yme porphobilinogen deaminase, also known as hydro0ymethylbilane synthase.

??. 1 The spinothalamic tract is a sensory pathway originating in the spinal cord. t transmits information to the thalam"s abo"t pain, temperat"re, itch and cr"de to"ch. The pathway dec"ssates at the le!el of the spinal cord, rather than in the brainstem like the posterior col"mnmedial lemnisc"s pathway and corticospinal tract. The cell bodies of ne"rons that make "p the spinothalamic tract are located in the spinal ganglia. These ne"rons recei!e inp"t from sensory fibers that inner!ate the skin and internal organs. A. .eft Borsal col"mns # press"re, !ibration, to"ch and proprioception$ C. .eft, .ateral Corticospinal tract # !ol"ntary motor$

?E.1 8"ltiple endocrine neoplasia type * #also known as QPheochromocytoma and amyloid prod"cing med"llary thyroid carcinomaQ QPTC syndrome,Q and QSipple syndromeQ is a gro"p of medical disorders associated with t"mors of the endocrine system. The t"mors may be benign or malignant #cancer$. They generally occ"r in endocrine organs #e.g. thyroid, parathyroid, and adrenals$, b"t may also occ"r in endocrine tiss"es of organs not classically tho"ght of as endocrine.8ost cases of 81&* deri!e from a !ariation in the G1T proto-oncogene, and are specific for cells of ne"ral crest origin.The protein prod"ced by the G1T gene plays an important role in the T56-beta #transforming growth factor beta$ signaling system. @eca"se the T56-beta system operates in n"mero"s tiss"es thro"gho"t the body, !ariations in the G1T gene can ha!e effects in n"mero"s tiss"es thro"gho"t the body. 81&* generally res"lts from a gain-of-f"nction !ariant of a G1T gene ?-.1 Sensiti)ed T lymphocytes enco"nter antigen and then release lymphokines # leads to macrophage acti!ation. no antibody in!ol!ed. http3((en.wikipedia.org(wiki(6ile3T4cell4acti!ation.png

?9. 1 The s"spensory ligaments of Cooper play an important role in the change in appearance of the breast that often accompanies the de!elopment of inflammatory carcinoma of the breast in which blockage of the local lymphatic d"cts ca"ses swelling of the breast. @eca"se the skin remains tethered by the s"spensory ligaments of Cooper, it takes on a dimpled appearance reminiscent of the peel of an orange #pea" d<orange$. Carcinomas can also decrease the length of Cooper<s ligaments leading to a dimpling. ?H.1 Transcytosis is the process by which !ario"s macromolec"les are transported across the interior of a cell. Desicles are employed to intake the macromolec"les on one side of the cell, draw them across the cell, and e:ect them on the other side. Ihile transcytosis is most commonly obser!ed in cells of an epitheli"m, the process is also present elsewhere. @lood capillaries are a wellknown site for transcytosis, tho"gh it occ"rs in other cells, incl"ding ne"rons, osteoclasts and intestinal cells. 1g 3 ns"lin and Antibodies. ?7. B Peripheral ne"ropathy and C&S effects are associated with the "se of isonia)id and are d"e to pyrido0ine #!itamin @9$ depletion, b"t are "ncommon at doses of - mg(kg. Persons with conditions in which ne"ropathy is common #e.g., diabetes, "remia, alcoholism, maln"trition, = Dinfection$, as well as pregnant women and persons with a sei)"re disorder, may be gi!en pyrido0ine #!itamin @9$ #1+,-+ mg(day$ with isonia)id.

?9.AA 66U56G(GP6.......Angiotrensine constricts the efferent a. ....L.inc 56G....Linc 66

E+.AA The normal PG inter!al is from 1*+ ms to *++ ms in length. The dr"gs that most commonly ca"se first-degree heart block are those that increase the refractory time of the AD node, thereby slowing AD cond"ction. These incl"de calci"m channel blockers, beta-blockers, cardiac glycosides, and anything that increases cholinergic acti!ity s"ch as cholinesterase inhibitors. RRRCC@RRR The calci"m channel blockers known as

1. &on-dihydropyridines decrease the force of contraction of the myocardi"m s"ch as !erapamil or diltia)em, may be a!oided #or "sed with ca"tion$ in indi!id"als with cardiomyopathy. *.Bihydropyridine calci"m channel blockers are often "sed to red"ce systemic !asc"lar resistance and arterial press"re, b"t are not "sed to treat angina...s"ch as &efidipin 8any calci"m channel blockers also slow down the cond"ction of electrical acti!ity within the heart, by blocking the calci"m channel d"ring the platea" phase of the action potential of the heart. This res"lts in a negati!e chronotropic effect, or a lowering of heart rate. This can increase the potential for heart block.This res"lts in a negati!e chronotropic effect, or a lowering of heart rate. This can increase the potential for heart block.

E1.@@ Anti-dig 6ab fragments is an antidote for Cardiac glycosides to0icity

E*.BB Changes in the !ariables in Starling<s eC"ation can contrib"te to the formation of edema either by an increase in hydrostatic press"re within the blood !essel, a decrease in the oncotic press"re within the blood !essel or an increase in !essel wall permeability. The latter has two effects. t allows water to flow more freely and it red"ces the oncotic press"re difference by allowing protein to lea!e the !essel more easily.

E?.CC P pili mediate the binding of "ropathogenic 1. coli to a digalactoside receptor determinant present in the "rinary tract epitheli"m.

EE.BB &o !isible change by light microscopy in first *-E ho"rs.contraction bands !isible after 1-* ho"rs ..early coag"lati!e necrosis after E ho"rs.release of contents of necrotic cells into blood stream and the beginnig of ne"trophil emigration

E-.@@ &ormal portal press"re is generally defined between - and 1+ mm =g. =owe!er, once the portal press"re rises to 1* mm =g or greater, complications can arise, s"ch as !arices and ascites.Treatment is 1.by di"retic dr"gs *.by s"rgery to :oin the portal !ein to the inferior !ena ca!a #bypassing the li!er$ ?.implanting a stent within the li!er to :oin portal tract !eins to a hepatic !ein trib"tary #T PSS transc"taneo"s intrahepatic porto-systemic sh"nt$

E9.CC Cohort st"dy t is obser!ational and prospecti!e.....compares between a gro"p with a gi!en risk factors.#@"s dri!eres......dri!ing in seated position d"ring *+ years$ to a gro"p witho"t to assess #@"s condactors ...walking...$whether the risk factor increase the liklihood#8 $ of disease.

EH. B An esophageal motility st"dy #18S$ or esophageal manometry is a test to assess motor f"nction of the Mpper 1sophageal Sphincter #M1S$, 1sophageal body and .ower 1sophageal Sphincter #.1S$. ndications3 An 18S is typically done to e!al"ate s"spected disorders of motility or peristalsis of the esophag"s. These incl"de achalasia, diff"se esophageal spasm, n"tcracker esophag"s and hypertensi!e lower esophageal sphincter. These disorders typically present with dysphagia, or diffic"lty swallowing, "s"ally to both solids and liC"ids e!en initially. /ther patients with spasm disorders may ha!e the test done to diagnose chest pain tho"ght not to be of cardiac ca"se. The test is not "sef"l for anatomical disorders of the esophag"s #that is, disorders that distort the anatomy of the esophag"s$, s"ch as peptic strict"res and esophageal cancer. http3((en.wikipedia.org(wiki(1sophageal4motility4st"dy

E7. C Chronic 5ran"lomatosa Bisease3 .ack of &ABP= o0idase - decrease reacti!e o0ygen species# s"pero0ide$ and absent of respiratory b"rts in ne"trophils. ncrease s"sceptibility to catalase F organisms # S. A"re"s, 1. Coli, Aspergill"s$. &egati!e &itrobl"e tetra)oli"m dye red"ction test. #6A page *1*$ http3((en.wikipedia.org(wiki(Chronic4gran"lomato"s4disease

E9.@@

-+.@@