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 which may malf"nction as a res"lt. Acti!ation of the fibrinolytic system generates plasmin #in the presence of thrombin$. which carry deo0ygenated blood from the esophag"s to the a)ygos !ein. As the small clots cons"me coag"lation proteins and platelets.-.wikimedia. The small clots also disr"pt normal blood flow to organs #s"ch as the kidneys$.. which in t"rn drains directly into the portal !ein. which in t"rn drains directly into the s"perior !ena ca!a. as it is the central proteolytic en)yme of coag"lation and is also necessary for the breakdown of clots.* cm in diameter in association with portal hypertension. the respiratory tract and s"rgical wo"nds. from sites where blood samples were taken$.11 B C leads to the formation of small blood clots inside the blood !essels thro"gho"t the body. which drain into the coronary !ein #left gastric !ein$. or .11 consistent "se of CS6-PCG for =SD serology established a diagnosis in the ma:ority of ac"te aseptic meningitis patients. http3(("pload. These s"perficial !eins #normally only appro0imately 1mm in diameter$ become distended "p to 1. the gastrointestinal tract. which is responsible for the lysis of fibrin clots. The remaining blood from the esophag"s is drained into the s"perficial !eins lining the esophageal m"cosa.CC 1sophageal !arices are e0tremely dilated s"b-m"cosal !eins in the lower esophag"s.org(wikipedia(commons(b(b9(1sophageal4!arices. the presence of plasmin is critical. The ma:ority of blood from the esophag"s is drained !ia the esophageal !eins. These !eins ha!e no part in the de!elopment of esophageal !arices.. 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. commonly d"e to cirrhosis2 patients with esophageal !arices ha!e a strong tendency to de!elop bleeding. The breakdown of fibrinogen and fibrin res"lts in polypeptides called fibrin degradation prod"cts #6BPs$ or fibrin split prod"cts #6SPs$. They are most often a conseC"ence of portal hypertension. normal coag"lation is disr"pted and abnormal bleeding occ"rs from the skin #e. The fibrinolytic system then f"nctions to break down fibrinogen and fibrin. 9. n a state of homeostasis.g.4-4wale.:pg H. p-? is important in m"lticell"lar organisms. heart fail"re. where it reg"lates the cell cycle and. f the TP-? gene is damaged. Genin stim"lates the prod"ction of angiotensin . radiation. t can initiate apoptosis.i-6ra"meni syndrome. Angiotensin also stim"lates the secretion of the hormone aldosterone from the adrenal corte0. A The renin-angiotensin system #GAS$ or the renin-angiotensin-aldosterone system #GAAS$ is a hormone system that reg"lates blood press"re and water #fl"id$ balance. Aldosterone ca"ses the t"b"les of the kidneys to increase the reabsorption of sodi"m and water into the blood. and harmf"l effects of diabetes. or !ir"ses$. increasing the likelihood that the cell will begin decontrolled di!ision.J*KJ? Acti!ation .fibrinolysis. p-? works thro"gh se!eral mechanisms3 t can acti!ate B&A repair proteins when B&A has s"stained damage. kidney fail"re. These dr"gs are one of the main ways to control high blood press"re #hypertension$. :"0taglomer"lar cells in the kidneys secrete renin. The TP-? gene can also be damaged in cells by m"tagens #chemicals. genomic stability. This increases the !ol"me of fl"id in the body. There are many dr"gs that interr"pt different steps in this system to lower blood press"re. n its anti-cancer role. the programmed cell death. f the renin-angiotensin-aldosterone system is too acti!e. 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. which is then con!erted to angiotensin .@@ p-? is a t"mor s"ppressor protein that in h"mans is encoded by the TP-? gene. t"mor s"ppression is se!erely red"ced. Angiotensin ca"ses blood !essels to constrict. a disease known as . and plays a role in apoptosis. 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. People who inherit only one f"nctional copy of the TP-? gene will most likely de!elop t"mors in early ad"lthood. blood press"re will be too high. th"s. and inhibition of angiogenesis. 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$. which also increases blood press"re. Ihen blood !ol"me is low. 7. res"lting in increased blood press"re. if B&A damage pro!es to be irreparable. 8ore than -+ percent of h"man t"mors contain a m"tation or deletion 9. Angiotensin ca"ses blood !essels to constrict. bone resorption fails while its formation persists.11 /steopetrosis. deficiency of carbonic anhydrase in osteoclasts is noted. Aldosterone ca"ses the t"b"les of the kidneys to increase the reabsorption of sodi"m and water into the blood. called angiotensinogen. normal. renin-angiotensin aldosteron system 1+.AA Ihen blood !ol"me is low. 8ost importantly.. 1. or increased. ca"sing these cells to contract along with the blood !essels s"rro"nding them and ca"sing the release of aldosterone from the )ona glomer"losa in the adrenal corte0. con!erting it into angiotensin . and intracrine hormone. which also increases blood press"re.. Alternati!ely. ?. This increases the !ol"me of fl"id in the body. http3((en. res"lting in increased blood press"re.Ldec. an inacti!e peptide. Angiotensin is the ma:or bioacti!e prod"ct of the renin-angiotensin system. Angiotensin is then con!erted to angiotensin by angiotensin-con!erting en)yme #AC1$JEK which was tho"ght to be fo"nd mainly in l"ng capillaries.&ormal bone growth is achie!ed by a balance between bone formation by osteoblasts and bone resorption #break down of bone matri0$ by osteoclasts. a"tocrine(paracrine. a decrease in plasma &aCl concentration will stim"late the mac"la densa to release renin. as an acidic en!ironment is needed for dissociation of calci"m hydro0yapatite from bone matri0.org(wiki(Genin-angiotensin4system 9.J-K E. n osteopetrosis. Angiotensin also stim"lates the secretion of the hormone aldosterone from the adrenal corte0..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$. so when blood !ol"m is become higher by recei!ing 1 liter fl"id. =ence.. Angiotensin acts as an endocrine.. binding to receptors on intraglomer"lar mesangial cells.. =owe!er new e!idence s"ggests the AC1 is fo"nd in all blood !essel endothelial cells.. osteoclast dysf"nction mediates the pathogenesis of this disease. which is then con!erted to angiotensin .. *. Genin stim"lates the prod"ction of angiotensin . The absence of this en)yme ca"ses defecti!e hydrogen ion p"mping by osteoclasts and this in t"rn ca"ses defecti!e bone resorption by osteoclasts. . :"0taglomer"lar cells in the kidneys secrete renin. becoming denser. f the perf"sion of the :"0taglomer"lar apparat"s in the kidney<s mac"la densa decreases. also known as marble bone disease is an e0tremely rare inherited disorder whereby the bones harden. the n"mber of osteoclasts may be red"ced. then the :"0taglomer"lar cells release the en)yme renin. Genin clea!es a )ymogen.wikipedia. . /!erdose may also lead to p"lmonary edema and ac"te renal fail"re as a res"lt of shock. deafness =ematological diffic"lties.I 11... bradypnea."naffected Symptoms3Pain 6reC"ent fract"res...ele!ated Parathyroid =ormone."naffected Alkalin phosphatase. the main characteristic of phenobarbital o!erdose is a QslowingQ of bodily f"nctions. incl"ding decreased conscio"sness #e!en coma$. especially of the long bones. P/* N. incl"ding anemic thrombocytopenia. bradycardia.. incl"ding malformed and "nerr"pted teeth nfection @leeding Stroke 11. hypothermia. decreased respiration #hypo!entilation$ ca"ses increased blood carbon dio0ide and decreased o* and p= #a condition generally called acidosis$.10cessi!e bone is formed. blindness. . and hypotension #in massi!e o!erdoses$. le"kopenia 1nlarged spleen /steomyelitis 6rontal bossing of the sk"ll Mn"s"al dentition. B Gespiratory Acidosis3 Ph N. /steopetrosis 3 Calci"m..B Phenobarbital ca"ses a QdepressionQ of the body<s systems."naffected Phosphate... represented by the letters P . which often do not heal &er!e compression. leading to headache. mainly the central and peripheral ner!o"s systems2 th"s. PC/* O... This is d"e to profo"nd depression of the central ner!o"s system. Sleep dist"rbance *. bradycardia.? e8edicine med(*+H Phenobarbital ca"ses a QdepressionQ of the body<s systems. 5"ilt or feeling of worthlessness E. B 8a:or Bepressi!e Bisorder3 Characteri)ed by at least . hypothermia. Bepressed mood #6A page EE?$ . Appetite( weight changes H. and hypotension #in massi!e o!erdoses$. incl"ding decreased conscio"sness #e!en coma$. Symptoms m"st incl"de patient . The electroencephalogram of a person with phenobarbital o!erdose may show a marked decrease in electrical acti!ity. S"icidal ideations 9. to the point of mimicking brain death. the main characteristic of phenobarbital o!erdose is a QslowingQ of bodily f"nctions.oss of energy -. . mainly the central and peripheral ner!o"s systems2 th"s.RRRRRRRRRRRRRRRCorrectionRRRRRRRRRRRRRRR Ss 11 RRRRRRRRRRRRRRRRRRRRRRRRR @arbit"rate o!erdose Poisoning by barbit"rates Classification and e0ternal reso"rces CB-1+ TE*.report depressed mood or anhedonia3 1.oss of concentration 9. bradypnea. . Psychomotor retardation or agitation 7. and is "s"ally re!ersible.J*EK 1*.of the following 9 symptoms for * weeks. /!erdose may also lead to p"lmonary edema and ac"te renal fail"re as a res"lt of shock. loss of interest # anhedonia$ ?. ca"sing decrease "ric acid secretion and s"bseC"ent b"ild"p in blood. B 'ey answer is B and wo"ld go for B too. Crystals are needle shaped birefringentU yellow "nder parallel light TT/3 Colchicine.Accept the health beliefs of the patients a. classic manifestation is painf"ll 8TP :oint of the big toe # Podagra$. /ffer to e0plain things to family members for the patients. e!en if not technically precise. 10pect them. %oint is swollen. PGPP e0cess. allop"rinol. B0 need to be e0plained in the way patients can "nderstand. PGPP e0cess. and painf"l. c. Toph"s formation often on e0ternal ear.. 1?.esch &yhan Syndrome. #'aplan @S book page 1??$ 1?.&egociate3 &egotiate rather than order a. %oint is swollen. 6A page ?7+ RRRRRRRRRRRRRRRRRRCorretion RRRRRRRRRRRRRRRR 1E.. red... oleocranon b"rsa. Gelationship and agreement s"pport adherence. 6indidng3 Precipitation of monosodic "reate crystals into :oints d"e to hyper"ricemia. noy commands by the physician. oleocranon b"rsa.1?. @ 5o"t3 Asymetric :oint distrib"tion. #'aplan @S book page 1?1$ G"le T 19. B G"le T9. or achiles tendon. which can be ca"sed by . Toph"s formation often on e0ternal ear. classic manifestation is painf"ll 8TP :oint of the big toe # Podagra$. Treatment choices are the res"lt of agreement. ca"sing decrease "ric acid secretion and s"bseC"ent b"ild"p in blood.esch &yhan Syndrome. 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. probenecid. 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.. . &SA Bs. @e accepting of benign folk medicine practice. red. and painf"l. 6indidng3 Precipitation of monosodic "reate crystals into :oints d"e to hyper"ricemia. which can be ca"sed by . or achiles tendon. @ 5o"t3 Asymetric :oint distrib"tion.. b. E. the hemoglobin molec"les e0ist as single.et "s see what happens in sickle cell anemia.. and methionine gro"ped together with the protein... the molec"les tend to stick together and form long chains or polymers . s"ch as alanine. probenecid. isole"cine. phenylalanine..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.gl"tamic acid#hydrophillic $ is replaced by hydrophobic !aline #which increases the n"mber of hydrophobic aminoacids ...and hydrophobic interaction is between indi!id"al aminoacids H-/rdinarily.. &SA Bs.d"e to interaction between anionic carbo0ylate #GC//-$ and cationic ammoni"m #G&=?F$ in the amino acids b-hydrogen bonds.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. allop"rinol. 9-the hydrophobic effect is important to "nderstand the str"ct"re of proteins that ha!e hydrophobic amino acids.. whether they ha!e o0ygen bo"nd or not. 6A page ?7+ 1-. le"cine.1ach s"b"nit is composed of a protein chain tightly associated with a non-protein heme gro"p.Crystals are needle shaped birefringentU yellow "nder parallel light TT/3 Colchicine...salt bridges..which int"rn .. c.AA 1-=emoglobin is an assembly of fo"r glob"lar protein s"b"nits#polypeptide chains$.. and charged or polar side chains on the sol!ent-e0posed s"rface where they interact with s"rro"nding water molec"les... *. ?-1ach protein chain arranges into a set of alpha-heli0 str"ct"ral segments connected together in a globin fold arrangement.. 9-Ihen sickle hemoglobin releases o0ygen in the peripheral tiss"es.which is a nonco!alent bonding. 7-Sickle hemoglobin e0ists as isolated "nits in the red cells when they ha!e o0ygen bo"nd. isolated "nits in the red cell. howe!er..oil and water donot combine bec"ase of hydrophobic interaction . !aline..hydrophobic interactions... Dasc"lar and neoplastic #malignant or benign t"mo"rs$ lesions from the optic tract. SPB is not the same as schi)ophrenia. Posterior . tra"ma. C 5ardner syndrome. Thalam"s 1. epidermoid cysts. 6or e0ample. to !is"al corte0 can ca"se a contralateral homonymo"s hemianopsia. the more symmetric #congr"o"s$ the homonymo"s hemianopsia will be. and emotional coldness. also known as familial colorectal polyposis. "s"ally more congr"ent between the two eyes.increases hydrophobic interactions $ . as well as the occ"rrence of desmoid t"mors . fibromas and sebaceo"s cysts. infection. a person who has a lesion of the right optic tract will no longer see ob:ects on his left side.. n:"ry to the right side of the brain will affect the left !is"al fields of each eye. Similarly.and these hydrophobic interactions stabili)e the polymeri)ed sickle hemoglobin. or following s"rgery. 1H.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. 17. a person who has a stroke to the right occipital lobe will ha!e the same !is"al field defect. sometimes se0"ally apathetic. thyroid cancer. 19.. The more posterior the cerebral lesion. A stroke on the right side of the brain #especially parietal lobe$. Primary motor corte0 area C. Ca"date n"cle"s @. is an a"tosomal dominant form of polyposis characteri)ed by the presence of m"ltiple polyps in the colon together with t"mors o"tside the colon.. and there may be mac"lar sparing. in addition to prod"cing a homonymo"s hemianopsia.B =omonymo"s hemianopsia can be congenital.The e0tracolonic t"mors may incl"de osteomas of the sk"ll. secreti!eness. t"mors. altho"gh they share some similar characteristics s"ch as detachment or bl"nted affect and there is increased pre!alence of the disorder in families with schi)ophrenia.. A. may also lead to the syndrome of hemispatial neglect.1 Schi)oid personality disorder #SPB$ is a personality disorder characteri)ed by a lack of interest in social relationships. b"t is "s"ally ca"sed by brain in:"ry s"ch as from stroke.imb 19. a tendency towards a solitary lifestyle. 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 -$. n a small n"mber of cases. Ihen the term Q"rothelialQ is "sed. Polyps may also grow in the stomach. also "rothelial cell carcinoma or MCC$ is a type of cancer that typically occ"rs in the "rinary system3 the kidney. t is the most common type of bladder cancer and cancer of the "reter. reaching the "ter"s by tra!eling in the cardinal ligament. sessile #flat$ or carcinoma-in-sit" #C S$. The pattern of growth of TCCs can be papillary. li!er and kidneys. a more common disease that also predisposes to colon cancer. with ?+-E+> of patients ha!ing more than one t"mo"r at diagnosis. spleen. t commonly anastomoses #connects with$ the o!arian artery.1 The "terine artery "s"ally arises from the anterior di!ision of the internal iliac artery.years2 treatments are s"rgery and palliati!e care. E+> are in the spine. altho"gh some chemotherapy has been tried with limited s"ccess. The "terine artery is the ma:or blood s"pply to the "ter"s and enlarges significantly d"ring pregnancy. li!er. kidneys. The co"ntless polyps in the colon predispose to the de!elopment of colon cancer2 if the colon is not remo!ed.in appro0imately 1-> of affected indi!id"als. *+. meaning a TCC of the "rinary system. the chance of colon cancer is considered to be !ery significant. The most common site of TCC metastasis o"tside the pel!is is bone #?->$2 of these bone metastases. and in its more ad!anced forms. This is the same gene as is m"tant in familial adenomato"s polyposis #6AP$.E. "rinary bladder. At this time.B Transitional cell carcinoma #TCC. and "rach"s2 it is the second most common type of kidney cancer. t tra!els to the "ter"s. it specifically refers to a carcinoma of the "rotheli"m. TCCs are often m"ltifocal. TCC arises from the transitional epitheli"m. a tiss"e lining the inner s"rface of these hollow organs. t tra!els thro"gh the parametri"m of the inferior broad ligament of the "ter"s. Cancers related to 5S commonly appear in the thyroid. there is no c"re. mesentery and small bowel. . d"oden"m. 19. polyps ha!e also appeared in the cerebell"m. and accessory organs. it is considered a terminal diagnosis with a life e0pectancy of ?-. crossing the "reter anteriorly. "rethra. 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. 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.. &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. folding. 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. C.wikipedia. with effects on micro!asc"lar blood flow and tiss"e health. nitially. and pit"itary$. P.%P5 http3((en. 1C"imolar amo"nts of C-peptide and ins"lin are then stored in secretory gran"les of the pancreatic beta cells and both are e!ent"ally released to the portal circ"lation. b"t this !aries with the n"tritional state. whereas C-peptide le!els in type * patients are normal or higher than normal. the sole interest in Cpeptide was as a marker of ins"lin secretion and has as s"ch been of great !al"e in f"rthering the "nderstanding of the pathophysiology of type 1 and type * diabetes. The li!er e0tracts abo"t half the ins"lin reaching it in the plasma.and the @. of if they prod"ce any at all.org(wiki(6ile3@lasent"mor. C-peptide has been fo"nd to be a bioacti!e peptide in its own right. C-peptide is also "sed for determining the possibility of gastrinomas associated with 8"ltiple 1ndocrine &eoplasm syndromes #81& 1$. higher le!els of C-peptide together with the presence of a gastrinoma s"ggest that organs besides the stomach may harbor neoplasms. @ 6actitio"s =ypoglycemia #self in:ection of ins"lin$.http3((en. parathyroids. B"ring the past decade. 5l"cose . Since a significant n"mber of gastrinomas are associated with 81& in!ol!ing other hormone prod"cing organs #pancreas. ser!es as an important linker between the A. and processing of ins"lin in the endoplasmic retic"l"m. howe!er.. nc C peptide . ins"lin .:pg *1.wikipedia. C-peptide le!els are checked in women with Polycystic /!arian Syndrome #PC/S$ to determine .. dec.org(wiki(6ile3@ladder4"rothelial4carcinoma4#1$4pT1. C-peptide sho"ld not be conf"sed with c-reacti!e protein or Protein C..chains of ins"lin and facilitates the efficient assembly. dec &o ketoacidosis. fatig"e.This connection is called the hypothalamohypophyseal tract.. and dehydration which are 5 T Symptom *$ clinical latency..@@ . diarrhea.. the de!iations wo"ld be small. the greater the de!iations .. !omiting. and is responsible for the release of o0ytocin and antidi"retic hormone.. 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.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. *++7 **.All choices e0cept /0ytocin are hormones of anterior pit"itary *E.degree of ins"lin resistance.. according to the res"lts of a long-term s"r!i!al analysis reported in the /ctober 9. ?$ manifest illness.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..medscape.na"sea. anore0ia..f the scores were cl"stered aro"nd the mean. and E$ reco!ery or death my answer is 5 T here is the link http3((emedicine.. abdominal cramping.com(article(7?E+1--o!er!iew *?. b"t they wo"ld .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. @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.. 5ro"p A co0sackie!ir"ses tend to infect the skin and m"co"s membranes. rashes... pancreas. and li!er.BB .@@ ... and hand. 8"ffled heart so"nds and p"ls"s parado0"s are signs of this. ple"ra. the lower the !al"e of the SB.is an inde0 of !ariability3 the SB increases in !al"e as the distrib"tion becomes more !ariable.8idbrain .So to check !ariabilty#hterogeneity$ ..V . which also incl"des polio!ir"s and echo!ir"s.V. and aseptic meningitis...D .5ro"p @ co0sackie!ir"ses tend to infect the heart. *H.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.. ac"te hemorrhagic con:"ncti!itis #A=C$..D. pericarditis. ca"sing ple"rodynia....8ed"lla *9.low SB means low !ariabilty #less hetrogeno"s pop"lation $.D .. n"clei2p"pil contract bilateraly Cranial ner!e n"clei3 C& .. "pper respiratory tract disease. -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 . foot and mo"th #=68$ disease... Picorna!iridae and the gen"s 1ntero!ir"s.. The less the !ariability in the distrib"tion. and hepatitis #inflammation of the li!er not related to the hepatotropic !ir"ses$Co0sackie @ infection of the heart can lead to pericardial eff"sion.Pons ...V . n short when we get high SB that means high !ariabilty #high heterogeno"s pop"lation in this case$.increase as the scores became more spread o"t or more !aried...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.. myocarditis.. @oth gro"p A and gro"p @ co0sackie!ir"ses can ca"se nonspecific febrile illnesses.compare the standard de!iation !al"es not the mean of the e0periment. *-. -5enerally SB . V.... ca"sing herpangina. D.D . 8CD has no animal reser!oir. or destroy cells if B&A cannot be repaired.. ?1.BBDestib"locochlear ner!e. =andling ob:ects that ha!e the !ir"s on them #fomites$. *7. infecting only h"mans. dome-shaped. with a dimpled center. if "ntreated.8oll"sc"m contagios"m lesions are flesh-colored. =owe!er.hearing and balance ?+.The !ir"s commonly spreads thro"gh skinto-skin contact. a bloated feeling. Mnder normal circ"mstances. di))iness and sweating.. Picking or scratching the b"mps may lead to f"rther infection or scarring. witho"t porphobilinogen . and finishes back in the mitochondrion.8oll"sc"m contagios"m #8C$ 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$. and pearly in appearance.Iomen with an abnormal @GCA1 or @GCA* gene ha!e "p to an 9+> risk of de!eloping breast cancer by age 9+2 increased risk of de!eloping o!arian cancer is abo"t --> for women with @GCA1 m"tations and abo"t *-> for women with @GCA* m"tations. They are often 1. damaged B&A is not repaired properly and this increases risks for cancers.. proceeds into the cytoplasm.CC The d"mping syndrome is 8ost people are "nable to tolerate certain foods after gastric bypass. f @GCA1 itself is damaged..B Ac"te intermittent porphyria #A P$ is a rare a"tosomal dominant. *9.X which may ca"se nasea and !omiting. 1ating these foods can ca"se the Wd"mping syndrome.@GCA1 is e0pressed in the cells of breast and other tiss"e. This incl"des se0"al contact or to"ching or scratching the b"mps and then to"ching the skin.8oll"sc"m contagios"m is contagio"s "ntil the b"mps are gone-which. heme synthesis begins in the mitochondrion. diarrhea.millimeters in diameter.. may be "p to 9 months or longer. They are generally not painf"l.. especially foods with high s"gar or fat content. b"t they may itch or become irritated. Certain !ariations of the @GCA1 gene lead to an increased risk for breast cancer.D . can also res"lt in infection.11 @GCA1 is a h"man t"mor s"ppressor gene that prod"ces a protein called breast cancer type 1 s"sceptibility protein. where it helps repair damaged B&A. s"ch as a towel. . constipation..BB ACMT1 &T1G8 TT1&T P/GP=PG A. ?*.. The light chain of the to0in has protease acti!ity. and the metabolite porphobilinogen acc"m"lates in the cytoplasm... The light chain is able to clea!e endocytotic !esicles and reach the cytoplasm. Patients with A P are commonly misdiagnosed with psychiatric diseases. 6ollowing the attachment of the to0in hea!y chain to proteins on the s"rface of a0on terminals. S"bseC"ent treatment with anti-psychotics increases the acc"m"lation of porphrobiliogen. Symptoms of A P may incl"de abdominal pain..deaminase.P Painf"l abdomen pink "rine polyne"ropathy psychological dist"rbances precipitated by dr"g . The to0in m"st get inside the a0on terminals in order to ca"se paralysis. a necessary cytoplasmic en)yme... the to0in can be taken into ne"rons by endocytosis. th"s aggra!ating the disease eno"gh that it may pro!e fatal. Additional factors m"st also be present s"ch as hormones. and dietary changes that trigger the appearance of symptoms. a type of S&AG1 protein.. 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.protein. The S&AP-*protein is reC"ired for !esicle f"sion that releases ne"rotransmitters from the a0on endings #in partic"lar Acetylcholine$. dr"gs..B @ot"lin"m to0in is a protein prod"ced by the bacteri"m Clostridi"m bot"lin"m. and m"scle weakness.. ?1.A in "rine symptoms. and so pre!ents ne"ro-secretory !esicles from docking(f"sing with the ner!e synapse plasma membrane and releasing their ne"rotransmitters.ca"ses acc"m"lation of porphobilinogen and delta -A.J-7K @ot"lin"m to0in specifically clea!es these S&AG1s. heme synthesis cannot finish.. The type A to0in proteolytically degrades the S&AP-*.BM1 T/ MG/P/GP=PG &/51& SP&T=AS1 deficiency . also known as hydro0ymethylbilane synthase. parathyroid. http3((en. !ariations in the G1T gene can ha!e effects in n"mero"s tiss"es thro"gho"t the body. They generally occ"r in endocrine organs #e.A dehydratase#is degenerated by . The pathway dec"ssates at the le!el of the spinal cord. .g. temperat"re. These ne"rons recei!e inp"t from sensory fibers that inner!ate the skin and internal organs. rather than in the brainstem like the posterior col"mnmedial lemnisc"s pathway and corticospinal tract. The cell bodies of ne"rons that make "p the spinothalamic tract are located in the spinal ganglia.ateral Corticospinal tract # !ol"ntary motor$ ?E.8ost cases of 81&* deri!e from a !ariation in the G1T proto-oncogene. thyroid.eft Borsal col"mns # press"re. no antibody in!ol!ed.1 8"ltiple endocrine neoplasia type * #also known as QPheochromocytoma and amyloid prod"cing med"llary thyroid carcinomaQ QPTC syndrome.org(wiki(6ile3T4cell4acti!ation.Porphobilinogen #P@5$ is in!ol!ed in porphyrin metabolism. . and are specific for cells of ne"ral crest origin. The t"mors may be benign or malignant #cancer$.png . @eca"se the T56-beta system operates in n"mero"s tiss"es thro"gho"t the body. . t transmits information to the thalam"s abo"t pain. t is generated by aminole!"linate #A. to"ch and proprioception$ C. 81&* generally res"lts from a gain-of-f"nction !ariant of a G1T gene ?-. A. !ibration.ead poisoning$.The protein prod"ced by the G1T gene plays an important role in the T56-beta #transforming growth factor beta$ signaling system. ??. and adrenals$. b"t may also occ"r in endocrine tiss"es of organs not classically tho"ght of as endocrine.Q and QSipple syndromeQ is a gro"p of medical disorders associated with t"mors of the endocrine system.wikipedia.1 Sensiti)ed T lymphocytes enco"nter antigen and then release lymphokines # leads to macrophage acti!ation. 1 The spinothalamic tract is a sensory pathway originating in the spinal cord.A$ and the en)yme A.eft. P@5 is then con!erted into hydro0ymethyl bilane by the en)yme porphobilinogen deaminase. itch and cr"de to"ch. .. osteoclasts and intestinal cells.g. diabetes. The dr"gs that most commonly ca"se first-degree heart block are those that increase the refractory time of the AD node.mg(kg. alcoholism. Ihile transcytosis is most commonly obser!ed in cells of an epitheli"m...AA 66U56G(GP6.?9. maln"trition. These incl"de calci"m channel blockers..L. incl"ding ne"rons. draw them across the cell. @lood capillaries are a wellknown site for transcytosis. 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.Linc 66 E+. and e:ect them on the other side. cardiac glycosides. ?9. and anything that increases cholinergic acti!ity s"ch as cholinesterase inhibitors. b"t are "ncommon at doses of ... "remia.Angiotrensine constricts the efferent a. 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. Persons with conditions in which ne"ropathy is common #e. = Dinfection$. the process is also present elsewhere.. as well as pregnant women and persons with a sei)"re disorder. Carcinomas can also decrease the length of Cooper<s ligaments leading to a dimpling. 1g 3 ns"lin and Antibodies. it takes on a dimpled appearance reminiscent of the peel of an orange #pea" d<orange$. Desicles are employed to intake the macromolec"les on one side of the cell.. beta-blockers.. ?H. tho"gh it occ"rs in other cells.. may be gi!en pyrido0ine #!itamin @9$ #1+...-+ mg(day$ with isonia)id. ?7.AA The normal PG inter!al is from 1*+ ms to *++ ms in length.1 Transcytosis is the process by which !ario"s macromolec"les are transported across the interior of a cell. @eca"se the skin remains tethered by the s"spensory ligaments of Cooper. thereby slowing AD cond"ction. .inc 56G. RRRCC@RRR The calci"m channel blockers known as . This can increase the potential for heart block. E1. EE. The latter has two effects. This can increase the potential for heart block.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. *.@@ Anti-dig 6ab fragments is an antidote for Cardiac glycosides to0icity E*. coli to a digalactoside receptor determinant present in the "rinary tract epitheli"m.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 . by blocking the calci"m channel d"ring the platea" phase of the action potential of the heart. &on-dihydropyridines decrease the force of contraction of the myocardi"m s"ch as !erapamil or diltia)em.CC P pili mediate the binding of "ropathogenic 1. a decrease in the oncotic press"re within the blood !essel or an increase in !essel wall permeability. or a lowering of heart rate. E?.This res"lts in a negati!e chronotropic effect.. 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.contraction bands !isible after 1-* ho"rs .. This res"lts in a negati!e chronotropic effect. or a lowering of heart rate.Bihydropyridine calci"m channel blockers are often "sed to red"ce systemic !asc"lar resistance and arterial press"re.BB &o !isible change by light microscopy in first *-E ho"rs.s"ch as &efidipin 8any calci"m channel blockers also slow down the cond"ction of electrical acti!ity within the heart. may be a!oided #or "sed with ca"tion$ in indi!id"als with cardiomyopathy.1.. b"t are not "sed to treat angina. These incl"de achalasia.org(wiki(1sophageal4motility4st"dy E7. s"ch as peptic strict"res and esophageal cancer. or diffic"lty swallowing. "s"ally to both solids and liC"ids e!en initially.org(wiki(Chronic4gran"lomato"s4disease . /ther patients with spasm disorders may ha!e the test done to diagnose chest pain tho"ght not to be of cardiac ca"se.dri!ing in seated position d"ring *+ years$ to a gro"p witho"t to assess #@"s condactors .Treatment is 1.. These disorders typically present with dysphagia. http3((en.wikipedia.wikipedia. EH. n"tcracker esophag"s and hypertensi!e lower esophageal sphincter. C Chronic 5ran"lomatosa Bisease3 .. =owe!er.1S$.....decrease reacti!e o0ygen species# s"pero0ide$ and absent of respiratory b"rts in ne"trophils. B An esophageal motility st"dy #18S$ or esophageal manometry is a test to assess motor f"nction of the Mpper 1sophageal Sphincter #M1S$.. 1sophageal body and .implanting a stent within the li!er to :oin portal tract !eins to a hepatic !ein trib"tary #T PSS transc"taneo"s intrahepatic porto-systemic sh"nt$ E9. The test is not "sef"l for anatomical disorders of the esophag"s #that is..#@"s dri!eres.compares between a gro"p with a gi!en risk factors. complications can arise.walking.E-.CC Cohort st"dy t is obser!ational and prospecti!e.ower 1sophageal Sphincter #.. A"re"s. ndications3 An 18S is typically done to e!al"ate s"spected disorders of motility or peristalsis of the esophag"s.and 1+ mm =g.by s"rgery to :oin the portal !ein to the inferior !ena ca!a #bypassing the li!er$ ?. &egati!e &itrobl"e tetra)oli"m dye red"ction test... diff"se esophageal spasm.@@ &ormal portal press"re is generally defined between . ncrease s"sceptibility to catalase F organisms # S.by di"retic dr"gs *.$whether the risk factor increase the liklihood#8 $ of disease. #6A page *1*$ http3((en. disorders that distort the anatomy of the esophag"s$.ack of &ABP= o0idase . once the portal press"re rises to 1* mm =g or greater.. Coli.. Aspergill"s$. 1. s"ch as !arices and ascites. @@ -+.E9.@@ .