Gastrointestinal Flashcards

Question

Describe how you prevent travellers' diarrhoea

Answer 1

* reduce exposure to infectious agent via drinking purified water * antimicrobials * immunisation

Answer 2

* heart defects

Answer 3

blastocyst has a cavity called a blastocoele

Answer 4

* trophoblast * outer epithelial layer * forms extraembryonic structures of the placenta * inner cell mass

Answer 5

the inner cell mass splits via gastrulation into * epiblast (embryo) * hypoblast (extra embryonic tissue)

Answer 6

the epiblast forms 3 germ layers * Ectoderm * NS * epidermis * Mesoderm * blood * heart * kidneys * gonads * bones * muscles * CT * Endoderm * epithelium (i.e. of the gut)

Answer 7

* the notochord induces the overlying ectoderm to form the neural plate * the neural plate--\> neural groove--\> neural tube and neural crest cells

Answer 8

Neural crest cells migrate away from the neural tube to form a wide range of structures * dorsal root ganglia * symp and parasymp ganglia * enteric ganglia * schwann cells * melanocytes * dentine * and most notably the structures of the face) * **DEFECTS**--\> cleft lip and palate

Answer 9

* mesoderm= one of the 3 embryonic tissue types * mesenchyme= the shape and behaviour of the cells (NOT THEIR ORIGIN) * mesenchymal= cell have lose contants with each other and can move independently * epithelial= cells are connected to each other * NOTE: mesoderm is often in the form of mesenchymal tissue (can move independently) but the above terms are not interchangeable

Answer 10

* paraxial mesoderm (medial) * intermediate mesoderm * lateral mesoderm

Answer 11

* dermis of skin * axial skeleton * axial and limb muscles

Answer 12

* urogenital system

Answer 13

* ventrolateral body wall * limb skeleton * visceral pleura and peritoneum * vv * heart * wall of gut and resp tissues

Answer 14

* somitomeres appear down its length * at the 20 somitomere stage, the 8th pair becomes somites * after the 8th pair all of the rest become somites

Answer 15

* somite splits into: * sclerotome (axial skeleton) * dermomyotome splits into: * dermatome (dermis of skin) * myotome (axial and appendicular muscles)

Answer 16

* limb dev begins at the end of 4th week * its initiated by mesoderm * as the limb grows out it takes with it the surface ectoderm * ectoderm overlying the limb bud forms apical ectodermal ridge and now controls limb growth * feet and hands start off as symmetrical discs * digits are sculpted by apoptosis DEFECTS * splitting of ectodermal rigdge--\> diplopodia * failure of apoptosis sculting--\> syndactyly * amelia and meromelia (genetic or thalidomide) * congenital hip dislocation genetic

Answer 17

* a patch of mesoderm per limb that has the capacity to form a limb * if you remove the free limb patch the surrounding peribrachial cells can compensate * if you remove the whole patch no limb will develop * you can also transplant the free limb patch and get ectopic limb

Answer 18

a C-shaped tube

Answer 19

* first appears as a split in the lateral mesoderm * divides lateral mesoderm into splanchnic mesoderm (below) and somatic mesoderm (above) * yolk sac separates form the embryo with purse string * the space that becomes the lumen of the gut is pinched off * the anterior end of the space--\> foregut * posterior end--\> hind gut

Answer 20

* body wall * viscera

Answer 21

* before 3 weeks of dev, there is no mouth or anus * but oral pit (stomadeum) and anal pits (proctodeum) are present * after 3 weeks, oral plate (separates foregut from stomadeum) breaks and the oral cavity forms * ectoderm then meets endoderm

Answer 22

* anus is sealed by cloacal membrane * allantois forms as a branch of the hind gut * between the allantois and hind gut is the urorectal septum * the urorectal septum extends to divide rectum from the urogenital tract * the allantois gives rise to--\> bladder and urogenital tract

Answer 23

* pharyngeal arches are NOT gills! * the endodermal lining of the pharyngeal arches gives rise to a wide range of structures * there are 4 pharyngeal arches/pouch * arch 1= eustachian tube * arch 2= palatine tonsil * arch 3= parathyroid and thymus * arch 4= parathyroid, thymus and post brachial bodies (in thyroid)

Answer 24

* most of the heart is derived from the lateral splanchnic mesoderm * initially forms tubes bilaterally * the 2 endocardial tubes are brought together in the midline * fusion of the 2 tubes in the midline but not on the top or bottom (therefore 4 inflow/outflow vessels) * initial tube then folds and fuses to form 4 chambers of the heart DEFECTS * no consequence in fetus, but an issue immediately post birth * commonest= ventricular septal defects * failure to divide single ventricle into left and right * single ventricle is divided partly by ventricular septum * leaves intraventicular foramen

Answer 25

* at 1 month, GIT consists of foregut, hindgut and midgut which are still connected to the yolk sac by a yolk stalk * initially GIT is only as long as the foteus * it quickly lengthens and begins to buckle in midgut * it then rotates around axis of yolk stalk and superior mesenteric artery * fold large intestine across s intestine * further elongation of l intestine * growing gut is too big for body cavity and is therefore pushed into body stalk/outside of body wall * by week 9 the body cavity is finally big enough to hold it all and the gut retracts back DEFECTS * failure to retract gut back in--\> omphalocoele * retraction but failure to seal wall--\> umbilical hernia

Answer 26

* congenital defect where the body and organs are a mirror image to what they should normally be * stomach on left, liver, lung lobes, and heart sounds reversed * caused by defects in signals by cilia in the primitive node * instead of generating currents right to left, they generate currents left to right

Answer 27

* anterior and posterior axis determined by first cleavage * dorsal and ventral axis set by blastocyst * left and right set by primitive groove

Answer 28

* there are 3 stages of kidney development and therefore 3 types of kidneys * the kidney is from mesoderm NOT endoderm! * kidneys form low down then migrate up * 1st to appear= pronephros * it forms neprostomes and pronephric duct * nephrostomes degenerate and pronephric duct--\> mesonephros duct * mesonephros induces metanephros * mesonephros degenerates but leaves its mesonephric duct * ureters start budding off mesonephros at bladder * kidneys start their ascent

Answer 29

* the intial dev is identical between males and females * urogenital folds fuse together completely in males DEFECTS * partial fusion of urogenital folds in males--\> opening on base of penis (hypospadiasis)

Answer 30

* digestion * absorption * movement * protection * passive * imm system

Answer 31

* mucosa * submucosa * muscularis externa * serosa

Answer 32

* innermost layer * columnar or stratified squamous epithelium * supported by lamina propria (CT) containing nerves and vv * muscularis mucosae (thin layer of s muscle) * can be folded/invaginated forming glands

Answer 33

* beneath the mucosa * dense irregular CT * sometimes has glands * vv and nerves * function= provides strength and elasticity

Answer 34

* 2 layers of s muscle * inner circumferential layer * outer longitudinal layer * function= peristalsis

Answer 35

* outside surface of the gut * layer of CT to bind GIT to surrounding structures or periotneal cavity * simple squamous epithelium * non stick surface

Answer 36

* myenteric plexus * between longitudinal and circular muscular layers in muscularis externa * submucous plexus * lies in submucosa

Answer 37

* stratified squamous epithelium * submucosal glands (lubrication) * muscularis externa here is mix of skeletal muscle and s muscle * function= transport

Answer 38

* muscular sac * divided into * cardiac region * fundus * body * antrum * pyloric sphincter controls release of materials into intestine * function= initiates digestion, mechanical and chemical breakdown, regulates release of chyme, only MINIMAL absorption * secretes pepsinogen which--\> pepsin at low pH (2)

Answer 39

* simple columnar secretary epithelium * prominent muscularis mucosae * thick submucosa * thick muscularis externa (3rd oblique layer) * rugae (allows expansion) * gastric pits leading to gastric glands

Answer 40

* gastric surface cells: mucus * neck cells: mucus * regenerative (stem) cells * parietal (oxyntic) cells: HCl * zymogenic (chief) cells: pepsinogen

Answer 41

* mucosa is protected by the layer of mucus * its constantly being secreted

Answer 42

* longest part of the gut * divided into: duodenum, jejunum, ileum * simple columnar epithelium with microvilli (brush boarder) * villi are on plica circulares * crypts of leiberkuhn * function=completes digestion and absorbs products

Answer 43

by a factor of 20

Answer 44

by a factor of 2-3

Answer 45

by a factor of 10

Answer 46

* penetrate into the lamina propria * secrete fluid and mucus * goblet cells * stem cells

Answer 47

* extends into the core of each villus * contains s muscle, vv, lymphatics, imm cells, goblet cells * muscularis mucosae can move the villus

Answer 48

* short 25cm * **low** plica circulares * **few** goblet cells * receives secretions form gall bladder and pancreas * receives acid chyme with active pepsin * **Brunner's glands** in submucosa release alkaline mucus * **pH is raised** to 7.3

Answer 49

* jejunum * more plica * shorter villi * lots of goblet cells * Ileum * smallest villi * **peyer's patches**

Answer 50

* consists of: appendix, colon, rectum, anus * colon= very short * function= compacts faeces and recovers water and electrolytes

Answer 51

* similar structure to rest of gut except there are longitudinal muscle in 3 distinct strips= taenia coli * surface is smooth (no villi) * many crypts of Leiberkuhn

Answer 52

Visceral peritoneum * surrounds abdominal viscera Parietal peritoneum * lines the walls of the cavity

Answer 53

* External oblique * outer layer * front pockets orientation * overlaps costal margin up to edge to edge with pec major and serratus anterior * attaches to anterior half of iliac crest as far as ASIS then jumps to the pubic tubercle * has a free inferior edge= inguinal ligament (turned upwards and in on itself) * Internal oblique * middle layer * back pockets orientation * attaches directly to costal margin * meets the external oblique in the midline at the linear alba * attaches to the iliac crest as far as ASIS and its lowermost fibres attach to the inguinal ligament * lowermost fibres then insert into the pubic crest * Transversus abdominus * deepest layer * horizontal fibre orientation * underlaps the costal margin * meets in the midline at the linear alba * upper fibres attach to the iliac crest, and lower most fibres attach to the inguinal ligament * then they arch upwards and insert into the pubic crest by a conjoined tendon

Answer 54

rectus abdominus * vertically orientated either side of the midline * as they ascend from the pubic crest they diverge * the attach to the costal cartilage going up edge to edge with pec major * long fibres= not very powerful therefore there are 3 tendinous intersections * one at level of umbilicus * one at level of xyphi sternum * one in between * lies in an envelope made from 3 aponeurousus * above the umbilicus: the internal oblique fascia splits around it * below the umbilicus: all fascia go in front of it

Answer 55

* superior epigastric * branch of internal thoracic artery * supplies the top half * inferior epigastric * branch of external iliac artery * superficial epigastric artery * not really part of main supply * NOTE: they all run in the posterior part of the rectus sheath and run deep to rectus abdominus

Answer 56

* superifical and deep veins are present * dual venous drainage * portal venous system * systemic venous system

Answer 57

* inguinal ligament * lacunar ligament * pectineal ligament

Answer 58

* they develop on the posterior wall high up in extra peritoneal fat * the skin and superficial fascia are continuous with the scrotum * when the testes descend they need to go through multiple layers * transversalis fascia via the deep inguinal ring * move medially * under the arching fibres of transversus abdominus muscle and internal oblique = inguinal canal * external oblique via the external/superficial inguinal ring * as they descend they take their neurovascular supply with it, therefore gaining 3 layers of coverings * internal spermatic fascia (from internal oblique) * cremasteric fascia (from internal oblique and transversus abdominus) * external spermatic fascia (from external oblique)

Answer 59

* protrusion of abdominal contents through the abdominal wall during rising intra-abdominal P from anterior abdominal muscles contracting * often through the inguinal canal

Answer 60

Psoas major * in paravertebral gutters * next to lumbar vertebrae * attachments to bodies and transverse processes from T12--\>L5 * fibres converge and pass beneath inguinal ligament to attach to the lesser trochanter of the femer Psoas minor * only present in 2/3rds of ppl * long slender tendon with short slim belly * its genetically degenerating * it doesn't insert anywhere. i.e. it blends with the periosteum of the pelvis Quadratus lumborum * attaches to 12th rib, tip of transverse processes and posterior 1/2 of iliac crest below Iliacus * inverted triangle shaped * inferiolaterally * edge to edge with psoas * attaches to the iliac fossa, fibres converge to pass beneath inguinal ligament and then to attach to the lesser trochanter of the femor with psoas major to form the conjoined tendon= iliopsoas Illiacus

Answer 61

* Posterior layer * attached to the tip of spinous process * Middle layer * attached to the tip/middle of the transverse process * Anterior layer * attached to the front of the transverse process * All fuse laterally at the line of the 12th rib * gives attachment to anterior abdominal muscles * anchors transversus abdominus and internal oblique * Makes 2 compartments * anterior compartment: encloses quadratus lumborum * posterior compartment: encloses erector spinae muscle

Answer 62

* retroperitoneal * lateral to the vertebral column in paravertebral gutters on quadratus lumborum * extending from T12--\> L3 * anterior to the 12th rib * the right sits lower because of the liver * kidneys move on respiration

Answer 63

* 10cm long, 5 cm wide, 2.5 cm thick * supra-adrenal glands on superior aspect * asymmetrical * left side= crescent shaped * right side= party hat * divided into cortex (pale, outer) and medulla (pyramids, apex towards hilum) * surrounded by perirenal fat * fibrous capsule * renal fascia encloses perirenal fat * hilum face anterio-medially * vein, artery, duct are embedded in fat in the space within the kidney= renal sinus * single renal artery on both sides divides into 5 segmental arteries therefore has functionally distinct renal segments * multiple renal veins uniting to form a single renal vein that goes into the IVC (right goes straight to IVC, left crosses the front of the abdominal aorta then enters IVC) * renal pelvis/ureteric pelvis (funnel shaped structure) * most posterior structure at hilum * in embedded fat * receives 2-3 major calyces --\> ureters

Answer 64

* muscular tubes that pass urine from kidney--\> bladder * 25-30cm long * descends on psoas major * closely associated with the tips of the transverse processes * then runs over the pelvic brim and along the inside wall of the pelvis to pass obliquely into the bladder.

Answer 65

* metabolic * increase cortisol, ACTH, decrease insulin, albumin * physiologic * fever * decrease appetite inflammation * increase COX2, NO, PLA-2, cytokines and chemokines * haematologic * increase neutrophils, phagocytosis * immunologic * CD4 T cell activation * TH17 differentiation * DC maturation * NK cell activation * B cell activation

Answer 66

* gene segment= inactive IL-1beta precursor (31kDa) * N termunus segment is cleaved off by ICE (aka caspase-1) * C terminus part is the active IL-1beta (18kDa)

Answer 67

* rare disease where patients develop local and systemic signs of acute inflammation when they are exposed to cold * single nucleotide mutation of cryopyrin gene * cryoporin is a member of the NOD-like receptor family

Answer 68

* activation of inflammasomes requires 2 signals since pro-IL-1beta gene needs to be transcribed * priming signal= TLR or cytokine receptors are activated and activate NFk-beta which causes the transcription of pro-IL-1beta * activation signal= bacteria or toxins or viral RNA activate NOD-like receptors * activation of NOD-like receptors--\> induces the formation of inflammasome (complex of caspase-11, pro-caspase-1, ASC, cytosolic NLR) * inflammasome complex activates caspase-1 * caspase-1 cleaves pro-IL-1 * IL-1 is released * NOTE: the cell can only undergo inflammasome activation once because it then dies by pyroptosis

Answer 69

* caused by consumption of purine * rich foods (meat, alcohol) * monosodium-urate formation exceeds renal clearance capacity * therefore it precipitates into crystals that often lodge in joints * the innate imm system can recognise the crystals and phagocytose them * the crystals once inside can be recognised by NOD-like receptor 3 * this causes the activation of inflammasomes and then the production of IL-1 * therefore promoting acute inflammation (redness, heat, pain, swelling, loss of function)

Answer 70

* it is an IL-1 receptor antagonist * it will decrease acute inflammation and can therefore prevent gout * contraindication in neutropenia because it will increase the risk of infection (i.e. it further suppresses the already compromised imm system)

Answer 71

* salmonella is taken up by M cells but can then escape them to enter the blood stream * salmonella is an intracellular pathogen and therefore activates inflammasomes via its flagellin protein if it hasn't downregulated its flagellin quick enough once its inside the cell * inflammasomes are activated---\> activated caspase-1--\> IL-1 release--\> pyroptosis and release of salmonella * neutrophils can then phagocytose the salmonella and kill it * pro-IL-18 can also be activated by caspase-1--\> IL-18 release from cell--\> acts on CD8 T cells --\> they release IFN-gamma

Answer 72

* inflammasomes are activated in metabolic syndrome * IL-1 is produced which promotes insulin resistance of adipocytes and hepatocytes * this causes the pancreas to secrete more insulin which in turn can cause more insulin resistance * eventually the pancreas is exhausted --\> TII Diabetes * inflammasome and IL-1 activation can also play a role in atherosclerosis

Answer 73

* inflammation of the liver * Types * acute disease (weeks--\> months) * non-specific, flu like symptoms jaundice, dark urine, pale faeces * chronic disease (years--\> lifetime) * general malaise cirrhosis, liver cancer * fulminant disease (like a lightening strike)

Answer 74

* in hepatocytes * damage * jaundice from hyperbilirubinemia * cirrhosis from chronic liver damage * hepatocellular carcinoma

Answer 75

* disease is **IMMUNE-MEDIATED** * NOT cytolytic * there are age-related outcomes * early exposure= less severe acute disease but higher rates of chronic infection

Answer 76

* HAV= infectious hepatitis * HBV= serum hepatitis * HCV= serum non-A non-B * HDV= dependent on HBV * HEV= enteric non-A non-B * they are all unrelated to each other, from totally diff virus families * there is no cross protection * other causes= Hepatitis F,G,TTV and HSV, CMV, HIV, EBV, VZV

Answer 77

* picornaviridae family * hepatovirus * non-enveloped +sense ssRNA virus * resistant to stomach acid * encodes a single polyprotein * single serotype worldwide (great for vaccines) * replicates in intestinal epithelia--\> blood--\> replicates in liver (_primary_ site of replication)--\> shed into bile and faeces --\> contaminates water and food

Answer 78

* ALT rises * viral Ags rise * IgM anti-hepatitis virus rises * switches to IgG anti-hepatitis virus

Answer 79

* serological tests via ELISA IgM IgG * rising titre= acute infection * nucleic acid tests * PCR from blood/faeces, but inferior to ELISA

Answer 80

* sanitation * immune globulin * pre * post exposure (within 14days) Treatment * supportive therapy (rehydration and nutrition) * inactivated vaccine

Answer 81

* inactivated whole virus via formalin * alum adjuvant * highly effective * expensive to produce because you need diploid cells and testing to ensure the virus is actually inactivated

Answer 82

* Hepeviridae family * formerly Caliciviridae * hepevirus * non-enveloped icosahedral shaped +sense ssRNA * more fragile than HAV * there is minimal person-person transmission unlike HAV * the pathogenesis is poorly understood but is probably similar to HAV * lives in Kupffer cells and hepatocytes * secreted in faeces 2 weeks before and 1 week after symptoms

Answer 83

* symptoms= jaundice, cholestasis, malaise, anorexia, abdo pain, hepatomegaly, nausea and vomiting, fever, pruritus

Answer 84

* serology * nucleic acid assays * immune EM * culture

Answer 85

* sanitation * immune serum globulin is NOT effective Treatment * supportive therapy * NO vaccine or specific antivirals

Answer 86

-HBV -HCV -HDV

Answer 87

* there are 2 types of particles * doubled walled structure with outer envelope and inner capsid (INFECTIOUS PARTICLE) * incomplete HBsAg particles with only envelope proteins * it has a dsDNA genome in a relaxed incomplete ds circle bound with viral polymerase * there are 2 short DR and a capped RNA primer * the dsDNA genome has several RNA transcription start sites but one termination polyA site therefore you get diff proteins of diff lengths

Answer 88

* virus infects cell via fusion * outer lipid envelope is lost * enters nucleus * in attempt to repair incomplete circlular genome it makes cccDNA episome--\> pregenome RNA * pregenome RNA undergoes reverse transcription--\> dsDNA (still an incomplete circle) * Reverse transcription is a good target for drugs because it doesn't happen in our cells

Answer 89

* it **PENETRATES into mucosal epithelia** where it can then enter the blood (DOESN'T REPLICATE HERE) * it only **replicates in the liver**!!

Answer 90

* sequelae= chronic carrier, immune mediated liver damage, cirrhosis, liver failure, primary hepatocellular carcinoma (after 10-30 years)

Answer 91

* Acute HBV infection with recovery * IgM anti-HBc (core Ag) and anti-HBs (surface Ag) levels increase * surface Ag levels decrease in recovery * Chronic HBV infection * IgM anti-HBc increase but then wane over time * HBs Ag increase and remain high

Answer 92

* there is usually partial integration of the HBV genome into host cells * repeated hepatocyte destruction and regeneration --\> accumulation of chromosomal mutations--\> cancer

Answer 93

Serological tests measuring: -HBs Ag: infection -Anti-HBs Ig: recovery, immunity or previous vaccination -anti-HBc IgM: acute infection -anti-HBc IgG: past or chronic infection -HBe Ag: active replication of virus and therefore effectiveness of therapy -Anti- HBe Ig: virus is no longer replicating -HBV-DNA: active replication, more accurate than HBe Ag

Answer 94

* IFN-alpha (pegylated form) * nucleoside and nucleotide analogues (Lamivudine: nucleoside, Adefovir: nucleotide)

Answer 95

* subviral particles purified form yeast with an alum adjuvant * need 2-3 doses * protects against HBV and HDV * can be effective post exposure

Answer 96

* (aka delta virus) * delta Ag * HBs Ag (hepatitis B surface Ag= reason why HBV vaccine is protective against this) * ssRNA 70% self complementary--\> rolling circle replication

Answer 97

* only infects IN CONJUNCTION with HBV * there are 2 types of infections: * Coinfection with HBV (2 at the same time) * severe acute disease * low risk of chronic infection * Superinfection of HDV into HBV positive patients * develop chronic HDV infection * high risk of severe chronic liver disease

Answer 98

* 80% of infections occur via IVDU * initial infection may be asymptomatic but results in a life long chronic infection in 70% of ppl * only 30% of ppl clear the virus * its the leading drive for liver transplantation * no vaccine available but antiviral drugs are available * ppl have poor immunity * ss linear + sense RNA * from the Flavivirus family * has a high mutation rate * many genotypes

Answer 99

* RNA genome * nucleocapsid core * lipid envelope * lipid droplets attached to envelope glycoprotein 1 and 2 genome * * 5'UTR called the internal ribosomal entry site and 3' UTR * region encoding the polyprotein precursos is divided into structural protein region and nonstructural protein region * key proteins= * NS1= viroporin (nuclear pore) * NS2= transmembrane protein * NS3= enzymes * NS5A= IFN-resistance gene * NS5B= RNA dependent RNA pol

Answer 100

* binds to receptors on host cell surface * put into endosome * endosome is acidified and virus is uncaoted and escapes endosome * +sense RNA goes directly to the ER to be translated * RNA polymease is highly error prone and therefore leads to a high degree of genome diversity -gains surface proteins and coat * maturation * leaves cell

Answer 101

* chronic sequelae= liver fibrosis, cirrhosis, liver failure, primary hepatocelluar carcinoma

Answer 102

* IFN-alpha (pegylated) * Ribavirin= no effective for all and significant SEs * DAA * NOTE: you get better results with combination therapy

Answer 103

* viral entry inhibs * HCV RNA translation Inhibs * Post translational processing inhibs * NS3-4A protease inhibs) * HCV replication inhibs * NS5B pol inhibs * HS5A inhibs * helicase inhibs * cyclophilin B inhibs * viral assembly and release inhibs

Answer 104

a plant/animal that lives on/in another living organis on which it is METABOLICALLY DEPENDENT

Answer 105

host in which the parasite reaches sexual maturity

Answer 106

host in which development occurs but the parasite does NOT reach sexual maturity

Answer 107

host in which the parasite enters the body and does NOT undergo development but remains infective

Answer 108

an animal which can be normally infected with a parasite that also infects ppl

Answer 109

* Ectoparasites * lice * mites * ticks * Protozoal parasites * Entamoeba histolytica * Giardia intestinalis * Toxoplasma gondii

Answer 110

* Insects * flies and mosquitos * fleas * lice * Arachnids * mites * ticks

Answer 111

* Pediculus humanis/capitis * Phthirus pubis * obligate blood sucking parasite * infection= pediculosis * P.humanis= body louse, clothing spread of eggs * P.capitis= head louse, spread by contact * P.pubis= crabs, spread by contact * Pubic and head louse attach nits to hair

Answer 112

* Sarcoptes scabiei * live in tunnels in epidermis * small (0.5mm) * lifecycle on single host * favours fingerwebs, elbows, axillae, genitals * spread by contact

Answer 113

* can be vectors of infectious agents (viral, rickettsial, bacterial, protozoal) * some cause ascending paralysis * humans are rarely natural hosts but many will feed on humans (only females take blood meal) * Ixodes holocyclus * NOTE: Lime disease is NOT recognised in Oz

Answer 114

* amoeba * invades tissues in colon to cause amoebiasis * faecal-oral route * can cause extra-intestinal infections (liver, brain abscess)

Answer 115

-flagellate primitive eukaryote -faecal-oral route -zoonotic transmission -asymptomatic carriage -has long lived cysts -often in possums -causes Giardiasis -symptoms= diarrhoea, acute or chronic malabsorption -diagnosis= cysts in faeces -treatment= Tinidazole, clean water, sewage treatment -re-infection is common

Answer 116

* obligate intracellular parasite * infects all mammals and many birds * most are from ingesting undercooked meat * infection persists for life * causes asymptomatic infection in immunocompetent * congenital infection can be serious * sexual reproduction occurs in cats * causes toxoplasmosis * symptoms= asymptomatic, CNS lesions, ocular disease in HIV, enkephalitis in babies when mum is infected DURING pregnancy

Answer 117

* roundworms * tapeworms * flukes

Answer 118

* Pinworms (Enterobius vermicularis) * Ascaris lumbricoides * Strongyloides stercoralis

Answer 119

* Echinococcus granulosus * Taenia * T. saginata * T. solium

Answer 120

* Schistosoma mansonii

Answer 121

* most children will be infected at some time * 1cm long female crawls out of anus at night to release eggs * finger and sheets are contaminated

Answer 122

* eggs ingested by humans * larvae hatch in s intestine * adults in lumen of caecum (females are larger) * mating occurs * females migrate to perianal region at night to lay eggs * eggs on perianal folds, larvae inside eggs mature within 4-6hrs * cycle starts again when fingers are in bottom etc

Answer 123

* large intestinal roundworm * female lays 200,000 eggs/day * embryonisation occurs in soil r

Answer 124

* infection by skin penetration (wear shoes) * bronchotracheal migration * female produces 50 ova/day * embryonisation in colon * autoinfection occurs (i.e. it can complete its lifecycle inside the human host) * immunosuppression may cause dissemination * it can become coated with gram -ve bac

Answer 125

* lives in intestinal veins * eggs cause immunopathologic disease * transmitted by fresh water snails * acquired by bathing/working in fresh water * larva= cercaria penetrates skin

Answer 126

* zoonotic infection * humans are accidental intermediate hosts * tapeworm= less than 5mm in length * larval cysts= hydatid cysts * proliferation occurs internally in cysts producing infective protoscoleces

Answer 127

* Taenia saginata * Taenia solium * cestode parasites * cause cysticercosis in their intermideate hosts * can also cause neurocystercercosis * zoonotic infection * humans can be both definitive and intermediate hosts * tapeworm = up tp 10m long

Answer 128

* X-rays * absorption depends on * thickness of tissue * density of tissue * atomic number * absorption is improved by * adding a contrast medium e.g. Barium meal or IV contrast medium * using a more sensitive method e.g CT scan with iodine * gamma rays * emitted by radioisotopes introduced into the body * detected by a gamma camera * radioisotopes are attached to molecules * ultrasound * uses echoes returned from tissue interfaces * produces thin sectional images * there are different shapes of probes used on the skin * e.g. Doppler ultrasound * uses doppler effect * perceived change in frequency of waves when there is a relative movement b/w source of wave and observer of wave * allows you to detect BF * direction and speed * MRI * patient is put into a strong magnetic field * pulses --\> changes in magnetism * you listen for resulting singla * produces sectional images in ANY plane * PET

Answer 129

* digestion * absorption * excretion of waste * prevention of invasion by pathogens * epithelial barrier * acid * contains microbiome

Answer 130

* local control * via ENS and ICC * regulates contractile activity * regulates secretion of water and salt * endocrine control * singalling from intestinal mucosa--\> ancillary organs e.g. brain, pancreas, gall bladder * essential for secretion of enzymes and solvents * regulates appetite * vago-vagal reflex pathways * controls movements in upper GIT * control of swallowing * regulates acid secretion in stomach * coordinates contractions of stomach and duodenum * intestino-intestinal reflexes * some mediated by vagus others mediated by dorsal root ganglia and spinal cord * viscerofugal neurons from GIT --\> pre-vertebral sympathetic ganglia produce reflex inhibition of proximal regions when distal regions are distended * CNS control * mood * anticipation * activity

Answer 131

Interstitial Cells of Cajal * = modified s muscle cell * produces a rhythmic change in MEMPOT * connected by gap junctions * located within circular smooth muscle layer

Answer 132

* there are many diff types depending on their mediators * CCK, secretin, somatostatin, GLP1,2... * span epithelium * e.g. * serotonin containing enterochromaffin cells (EC) * enterochromaffin cell-like cells (ECL) * release histamine

Answer 133

Cephalic phase * triggered by: sight, smell, thought and taste of food * causes * salivation * 30% of all gastric acid secretion * pepsin secretion * receptive relaxation * operates via **vagus** * sets up stomach to store food

Answer 134

* 4 mediators interact * **Ach** from ENS excited by vagal efferent neurons * **Gastrin** from G cells in antrum and duodenum * **Histamine** from ECL cells, excited by Ach from ENS, inhibited by stomatostatin from D cells and duodenal D cells * **stomatostatin** inhibits parietal and G cells, stimulated by acid in duodenum and by gastrin

Answer 135

* moved down oesophagus to stomach via peristalsis * entirely neural control via vagus * upper and lower oesophageal sphincters open and close * lower oesophageal sphincter is held closed at rest to prevent reflux * failure--\> GORD * fundus and corpus of stomach relax to accomodate change in vol * distension--\> activates enteric and vago-vagal reflexes * more acid and pepsin are secreted * ICC pacemaker activity propagates form corpus--\> antrum leading to ripples of contstriction --\> pylorus * food and acid enter antrum--\> triggers inhibition of acid secretion * strong constrictions form ICC drive food towards the closed sphincter--\> food separates especially fat * fat floats to fundus, forming a separate layer

Answer 136

* they decrease gastric acid **secretion** * PPI **kill** the enzyme, so you have to wiat for the synthesis of a new H/K ATPase pump * very potent * can let ulcers heal * e.g. * **omeprazole** * **esomeprazole**

Answer 137

* decrease gastric acid **secretion** * blocks histamine mediated gastric acid release * e.g. * **Ranitidine** * Cimetidine

Answer 138

* **neutralise** gastric acid * available OTC * all have SEs * therefore they are combined to decrease SE * some are constipative or laxative * all increase luminal pH therefore healing of ulcer can occur but you need to increase dose because gastrin will respond to increase acid seceretion= rebound hyperacidity * e.g. * sodium bicarbonate * (systemic action) * fizzy * **magnesium hydroxide/carbonate/oxide/trisilicate** * (not systemic) * laxative

Answer 139

* protects the ulcer site from acid * e.g * **sucralfate**

Answer 140

2 types * muscarinic receptor antagonists * decrease motility * anti-SLUD * e.g. * **hyoscine butylbromide** * no peripheral anti-muscarinic SE * direct spasmolytics * e.g. * peppermint oil * mebeverine

Answer 141

* increase mucus secretion and mucosal BF * decrease gastric acid secretion * e.g. * misoprostol

Answer 142

* H1 receptor antagonists * muscarinic receptor antagonists * e.g.: **hyoscine hydrobromide** * Dopamine D2 receptor angatonists * 5HT3 receptor antagonists * Neurokinin-1 (NK1) receptor antagonists

Answer 143

* supply * portal vein 75% * hepatic artery 25% * drainage * 3 main hepatic veins

Answer 144

* old way * falciform ligament divides the liver into left and right lobes * new way * draw a **line from the IVC to the gall bladder** * left lobe of liver is everything to the left of it

Answer 145

* polyhedral (6 surfaces) * 25um across * 1-2 nuclei * many cells are tetraloid or polyploid bc they are so busy making protein * prominent RER, golgi, secretatory vesicles, smooth ER, lots of mitochondria * they are epithelial cells

Answer 146

* lifespan= 150 days * replaced by division of **exisiting hepatocytes** * there are **NO** hepatic stem cells * capacity to regenerate is abolished by hepatitis B,C, or alcohol abuse (permanent damage)

Answer 147

* 75% of its weight is hepatocytes * hepatocytes are organised around vv (central vein and portal triads) * 2 blood supplies * venous blood from gut (hepatic portal system) * most of its blood is this deoxygenated blood * arterial supply * thin capsule= Glisson's capsule * hepatocytes are supported by reticular fibres (collagen type III) * hepatocytes are organised into lobules * lobules are organised into stacks/plates of hepatocytes * liver sinusoids * space of Disse

Answer 148

* 2 blood vessels and a duct * branch of hepatic portal vein * branch of hepatic artery * bile duct * BF outside of lobule--\> in * they give rise to a network of liver sinusoids * flow towards the middle of lobule * carry mixed oxygenated (20%) and deoxygenated (80%) blood

Answer 149

* its where all the sinusoids converge * carries blood to hepatic vein and out of liver * BF is ouside--\> in

Answer 150

* each plate of hepatocytes has a sinusoid above and below * sinusoids have incomplete walls therefore hepatocytes are directly bathed by escaped plasma * Space of Disse= extracellular space * therefore there is no barrier to what is in the blood

Answer 151

classic lobule * central vein is at centre hepatic lobule * hepatic portal vein and hepatic artery at centre * causes zonation * zone 1: **high** in O2, toxins, nutrients * zone 3: **low** in O2, toxins, nutrients * mirrors patterns in pathology

Answer 152

* produced by liver hepatocytes collected in cannaliculi (channels) in between hepatocytes * flows outwards to be collected into bile ducts in the portal triad * hepatic ducts join--\>common hepatic duct--\>common bile duct--\> through sphincter of Oddi--\> into s intestine * if sphincter of Oddi is closed the bile backs up and is stored in the gall bladder * consists of bile salts synthesised from cholesterol * they are reabsorped in the s intestine and recycled (90%) * bile= dark green due to bile pigament * bile pigament = breakdown product of Hb

Answer 153

* smooth muscle forms muscular sac * simple columnar epithelium (absorptive surface) * tough serosa

Answer 154

* **fat** in duodenum stimulates cells of duodenum to release **CCK** * CCK causes gall bladder to **contract** and **spincter** of **Oddi to relax** * bile squirts into duodenum

Answer 155

* its ducts drain into the common bile duct at the sphincter of Oddi * pancreatic juice contains: proteases, lipases, amylases, nucleases, bicarbonate ions * has endocrine (hormones) and exocrine (into ducts) parts * Islets of Langherans= endocrine parts * pancreatic glands are formed from acini * like a bunch of grapes with stems all connected * many of its enzymes are secreted as zymogens that are activated by other enzymes or bile salts * therefore if bile enters pancreas, it autodigests because of shared common route

Answer 156

acid activates D cells in the duodenum to release somatostatin

Answer 157

* activates D cells to release **somatostatin** * excits vagal afferent neurons to trigger vago-vagal reflex--\> **Brunner's glands to release mucus and bicarbonate** * vago-vagal reflex also **inhibits gastric emptying** * duodenal pyloro antral reflex **closes pylorus** and **inhibits gastric emptying**

Answer 158

* amino acids and fatty acids

Answer 159

* excites terminals of **vagal afferent neurons** * **satiety** factor acting on the hypothalamus * goes up to brain to control appetite * excites terminals of **enteric sensory neurons** within the gut wall * causes gall bladder contractions * forces **bile** down * releases **digestive enzymes** from pancreas

Answer 160

amino acids

Answer 161

* triggers **secretion of bicarbonate rich solution** from pancreas * enters duodenum via pancreatic duct * **neutralises gastric acid** * **inactivates pepsin** * **stops somatostatin secretion** from D cells * **removes brakes on gastric emptying** by terminating acid stimulated duodenal-antral reflexes and vago-vagal reflexes

Answer 162

* mediators released from basolateral surface * receptors are on apical surface

Answer 163

* **EC cells** express all the components of the taste pathways for **bitter and umami** * tastants cause release of **serotonin** from EC cells * **L cells** express **sweet** taste receptors * release **glucagon-like peptides 1 and 2, pancreatic polypeptide Y** * they regulate **appetite** (PYY) and **insulin** secretion * PYY can also act on **enteric neurons**

Answer 164

* changes from vagal to ENS circuits * retropulsion * towards pylorus * mixes pancreatic juices and bile with food * segmentation * local constrictions alternating with relaxation * mix food etc * brings nutrients to absorptive epithelium * peristalsis * propels content into new regions

Answer 165

* moves slowly via segmentation * occasional rapid peristalsis * digestion releases nutrients that activate EE and EC cells * rate of transit determines efficacy of digestion and absorption * gastric emptying continues * fat empties from stomach last giving a surge of CCK release

Answer 166

* mechanism is the same but stimuli change as digestion is completed * absorption of water--\> content is more viscous * in proximal colon, fermentation by microbiome --\> short chain FAs (acetate, butyrate, propionate) all stimulate enteric reflexes

Answer 167

* distension/stretch of rectum--\> urge to defaecate via sacral primary afferent neurons * mass movement contractions move contents from colon--\> rectum * requires conscious neural activity to relax anal sphincter and contract abdominal muscles * in IBS threshold of urge to defaecate is reduced and they can sense content that is not normally detectable

Answer 168

* aka migrating motor complex **(MMC)** * occurs in the **fasted** state * wave of constriction initiated in the antrum or upper duodenum slowly--\> ileo-colonic junction * only 1 MMC at a time * triggered by release of motilin * **clears bac and cellular debris** from otherwise empty lumen * failure= bac overgrowth

Answer 169

* **growth hormone release inhibitor** * released from **stomach in fasted state** * stimulates **appetite** * initiates MMC

Answer 170

* found **in nerve terminals** near G cells * acts in parallel to vagally released Ach

Answer 171

* polysaccharides= glucose polymers (starches and their derivatives) * dissaccharides= lactose and sucrose * dietary monosaccharides= glucose and fructose

Answer 172

* begins in the mouth with **salivary alpha-amylase** * hydrolyses **1:4**alpha linkages between glucose molecules * inactivated at acid pH in stomach * its reactivated in the duodenum when pH is returned to neutral via bicarbonate * **CCK** released from duodenal mucosa causes **pancreatic alpha-amylase** to be released * it enters the duodenum via the pancreatic duct * both types of amylases are ineffective at 1:6alpha linkages * the remainder of digesion happens at the **brush boarder membrane** * **isomaltase**: breaks **1:6 alpha linkages** * **sucrase**: breaks down sucrose * **maltase** * sucrase and maltase are synthesised as a large single glycoprotein that is then separated by pancreatic proteases

Answer 173

sucrose--\> glucose and fructose

Answer 174

* acts with sucrase and maltase enzymes * breaks down maltotriose and maltose

Answer 175

* glucose and fructose are rapidly absorbed across the mucosal epithelium * in the duodenum and jejunum * mainly at the **tips of the villi** * **glucose** * transport is **coupled to Na by SGLT1** * increased Na--\> increased glucose transport * enhanced by sweet taste receptor * **fructose** * transported by **GLUT5** by faciliated diffusion into epithelial cells * transported by **GLUT2** into interstitium

Answer 176

* begins in the stomach via **pepsin** * CCK release is triggered by aa--\> secretion of **pancreatic proteases** in the form of proenzymes * activated by enterokinase in epithelial membrane, which starts a cascade * eg. trypsinogen--\> trypsin * **pancreatic carboxypeptidases** (act at carboxy terminales to produce free aa) and * *aminopeptidases** are present * **brushboarder membrane enzymes**= mix of aminopeptidases, carboxypeptidases, endopeptidases and dipeptidases * break polypeptides--\> free aa * free aa are transported by 7 or more tranporters * 5 require Na, 2 of these also require Cl- * some di/tri peptides are transported dircetly into epithelial cells to be then broken down by **enterocyte small peptidases**

Answer 177

* secreted intially as **pepsinogens** from **chief cells** * **activated** by gastric **acid** * pepsinogen 1 secreted in acid secreting regions * pepsinogen 2 secreted closed to pylorus * hydrolyses bonds within the protein (not at the ends) (between aromatic aa and a 2nd aa) * produces diverse range of sizes * **inactivated** at **neutral pH**

Answer 178

* pancreatic proteases are endopeptidases * act at the interior bonds of peptides * produce short polypeptides * e.g. * trypsin * elastase * chymotrypsins

Answer 179

* starts in the mouth with **lingual lipase** * ****minor role * **gastric lipase** * minor role * but produce some FA to trigger CCK * CCK release--\> secretion of **pancreatic lipolytic enzymes** * **lipase** secreted in an inactive form * activated by colipase * colipase activated by trypsin * **cholesterol esterase** * activated by bile * hydrolysis of cholesterol ester * lipids are insoluble in water and need to be **emulsified by bile salts and lecithin** * micelles form * bile salts with lecithin, monoglycerides, FAs, cholesterol * lipids are brought to apical surface of epithelial cells at tips of villi * fat soluble lipids then dissolve in membranes and enter cells * **in cells** the FAs and monoglycerides **reform triglycerides** in the smooth ER * triglycerides are **coated** with apolipoproteins--\> **chylomicrons** * secreted by **exocytosis** * enter **lymphatics** * short chain FAs are also produced by **fermentation of dietary fibre** in the proximal colon * absorbed via **H dependent mechanism**

Answer 180

* mucus gel layer (bicarbonate rich) * hydrophobic monolayer (binds via its +vely charged head to -vely charged mucus gel layer) * underlying mucus cells are connected by tight junction

Answer 181

* its damaged by H.pylori, asprin, NSAIDs, bile, alcohol * release of histamine from underlying mast cells --\> inflammation * prostaglandins prevent and reverse mucosal injury * they inhibit acid secretion * stimulated HCO3-, mucus secretion, increase BF and modify local inflammation

Answer 182

* acute response to injury * **heals** within a few days due to rapid turn over and regeneration within 24-48hrs * response due to * chemical injury * drugs * stress * shock * burns * head injury * septicaemia * staphylococcal food poisoning * H.pylori --\> chronic gastritis * causes release of inflammatory mediators *

Answer 183

* oedema * erosion * coagulative necrosis of surface epithelium or submucosa * fibrosis * in severe cases you can get: * ulceration (damage to mucosal barrier) * an extension of erosions * stress ulcers * curlings ulcers * cushings ulcers * NSAID-induced ulcers * can occur in acute or chronic gastritis * haemorrhage * haematemesis * melena * blood loss

Answer 184

* A= Autoimmune * B= (bacterial) Helicobacter-associated * C= Chemical * others * granulomatous * lymphocytic * eosinophilic

Answer 185

* **immune mediated** destruction of **acid secreting tubules**--\> **atrophy** * tubules can be replaced by **intestinal and pyloric gland metaplasia** * **chronic inflammation** * with achlorhydria (no acid) * loss of intrisic factor--\> pernicious anaemia (B12 deficiency) * confined to gastric **corpus/body** mucosa * antrum is normal! * loss of acid and parietal cells--\> **hypergastrinaemia**(increased somatostatin)--\> linear and nodular **ECL hyperplasia** and sometimes **carcinoidosis** * there is circulating **autoabs** to parietal cell membrane **H/K ATPase, intrinsic factor and gastrin receptor**

Answer 186

* causes * **reflux of bile** and alkaline duodenal juice due to altered motility or gastro-jejunostomy * **long** term **use** of **asprin, NSAIDs** * direct mucosal injury= **disruption of mucus layer and gastric barrier, epithelial desquamation** * compensation **foveolar hyperplasia** (mucus secreting cells) * **elongation** and tortuosity of **gastric pits** * **vasodilation** * **oedema** * **fibromuscular hyperplasia** of lamina propria * only **mild inflammatory** cell infiltration * **erosions/ulcerations** * **intestinal metaplasia**

Answer 187

* **neutrophilic** gastritic/intraepithelial neutrophils present * neutrophilic and **lymphoplasmacytic** (lympocytes and plasma cells) infilitration of lamina propria * micro abscesses * **transient hypochlorhydia** (lack of stomach acid) present for up to 4 months * infiltration of **chronic inflamm cells** * **Abs** appear at 4 weeks but are not curative * **intestinal metaplasia** * gains **lymphoid tissue**--\>B cell lymphoma * Bac attaches under mucus barrier **to surface epithelium and tight juctions** to escape acid environment * secretes **urease** which breaks down urea in proteins to **release ammonium ions** * ammonium ions bind to bicarb--\> breakdown of mucus layer * bac also secretes **phospholipase**--\> damage phospholipid layer--\> acid and pepsin can now damage mucus layer--\> surface epithelium is exposed * permeability of epithelial cells--\> damage via acid leaking in

Answer 188

* normal mucosa--\> chronic gastritis from infection--\> atrophic gastritis--\> intestinal metaplasia--\> dysplasia--\> adenocarcinoma

Answer 189

* peptic ulcer disease * mainly causes duodenal ulcers (92% of the time) * 70% of gastric ulcers * gastric adenocarcinoma * gastric B cell lymphoma * iron deficiency anaemia * atrophic gastritis

Answer 190

its characterised by the presence of: * goblet cells * columnar absorptive cells

Answer 191

duodenal peptic ulcers= H.pylori (92%) gastric peptic ulcers= H.pylori (70%) and NSAIDs (25%)

Answer 192

* commenest= in 1st part of duodenum and antrum (ratio 4:1) * oesophagus at squamocolumnar junction/Z line * gastro-enterostomy stoma (operation joining stomach to jejunum) * Meckel's diverticulum

Answer 193

* a breach in the mucosa extending beyond the muscularis mucosae * due to digestion of mucosa by acid and pepsin * types * acute * superficial * heals * chronic * deep * destroys all layers fro muscularis mucosae--\> subserosa * scarring/fiborsis at the base--\> draws gastric folds to its margin--\>radial scar * partial restitution * gastric mucosa is replaced by intestinal and pyloric gland metaplasia

Answer 194

1. **exudate** of fibrin, neutrophils and necrotic debris 2. narrow zone of **fibrinoid necrosis** 3. zone of **cellular granulation tissue** 4. zone of **fibrosis** with endarteritis and hypertrophied nerves

Answer 195

* perforation * in anteriorly located ulcers * haemorrhage * erosion of an artery * haematemesis or melaena (rapid) * anaemia (slow) * penetration * erodes into an adjacent organ * stenosis * due to contraction of fibrous scar

Answer 196

* raised * thickened * infiltrated * NO radiating folds to margin * signet-ring cell carcinoma= cells dont adhere to each other

Answer 197

* coeliac sprue * gluten sensitive enteropathy

Answer 198

* immune mediated disease in genetically susceptible individuals (HLA-DQ2, HLA-DQ8) * driven by an environmental Ag, gluten found in wheat, rye and barley * results in chronic inflammation of the small bowel mucosa * remission that occurs on a gluten free diet is the hallmark of the disease * can manifest anytime from infancy to late adulthood

Answer 199

* dirrhoea * bloating * abdominal cramps * flatulence * anaemia * vitamin deficiencies * malabsorption * failure to thrive as an infant * osteoporosis * lethargy * migraines * infertility * mouth ulcers * increased prevalence of autoimm diseases * BUT many ppl can also be asymptomatic (but they still get the damage and increased risk of cancer!)

Answer 200

* 99.6% of cases are associated with HLA-DQ2, HLA-DQ8 * DQ peptide binding **cleft is +vely charged** and therefore binds -vely charged aa * Gliadins are rich in glutamine (+) * Unmodified gliadin peptides bind poorly * Gliadins modified by **tissue transglutaminase 2** cause glutamine (+)--\>glutamate (**-**) (=deamination) * Can now bind in pocket at positions **4,6 or 7**--\>Presented in MHC II in DCs to **CD4T cells**--\> Effector **TH1** response--\>Release **IFN-gamma, TNF-alpha, IL-4**--\>Damage * Gliadin causes epithelial cells to express **MIC-A and MIC-B (atypical MHC class I molecules) and release IL-15** --\> activation and proliferation of **IEL CD8 T cells** and also **lowered** TCR activation **threshold** * These **CD8T cells express NKG2D** (receptor for MIC-A)--\> IFN-gamma and enterocyte apoptosis * T cells can also cause B cell activation--\>Anti-gliadin and anti-tTG **Abs** (IgA or IgG) * Damage to enterocytes makes them more **permeable**, allowing more gluten to come across and more damage

Answer 201

1. genetics * -DQ2, -DQ8 2. environment * timing of gluten introduction * breast feeding is protective * infections 3. T cells * -DQ2, -DQ8 restricted CD4 T cells cause damage by IFN-gamma * CD8T cells accumulate 4. gluten * gliadins (45%) * glutenins (45%) * high content of glutamine and proline confers resistance to digestion by gut enzymes therefore it can cross the mucosa *

Answer 202

* villus atrophy/blunting--\> loss of brush boarder SA and enzymes--\> malabsorption * increased IELs * CD8 T cells * plasma cells * crypt elongation/hyperplasia * increased mitosis

Answer 203

* Type 1/ infiltrative * villous crypt length is normal. ratio 4:1 * increased IELs (\>30IELs per 100 enterocytes) * Type 2/ hyperplastic * elongation and branching of crypts * Type 3/ destructive * villi are shortened and blunted * villous to crypt ratio is less than 1:4

Answer 204

* tropical sprue * small bowel bac overgrowth * common variable immunodeficiency (CVID) * autoimm enteropathy * drugs (neomycin..)

Answer 205

* serological testing * tTG * deaminated gliadin peptide IgG * HLA-DQ haplotyping * small bowel biopsy * must be DURING gluten exposure * its the gold standard method for diagnosis

Answer 206

* osteoporosis * autoimmune diseases * cancer * small bowel lymphoma * (EATL) enteropathy assocaited t cell lymphoma * replacement of mucosa and submucosa by neoplastic T cells * small bowel adenocarcinoma * oesophageal cancer

Answer 207

* Bacteroidetes * Bacteroides * Prevotella * Firmicutes * Clostridia * Ruminococcus * Lactobaccillus * Actinobacteria * Bifidobacterium * Proteobacteria * E.coli NOTE: the distribution of these varies at diff sites

Answer 208

* metabolism * microbiota directly supply nutrients= vit B2, vit K, folate, biotin, lactose, cellulose) * microbiota alters metabolic machinary of host cells= bac degradation of host glycans--\> increase synthesis of new ones by host, produce short chain FA that maintain enterocyte differentiation, changes in host genes affecting angiogenesis and CHO and lipid metab * development * immune system * dev of mucosa associated lymphoid tissue * IgA and tolerance to normal microbiota and food Ags * protection against enteropathogen

Answer 209

* mode of baby delivery * vaginal delivery =rapid acquisition of Firmicutes, bifidobacteria * caesarian= delayed microbiota dev and restricted diversity * age * diversity increases with age * diet * high fat/low fibre--\> low fat/high fibre influences it * animal based diets decrease levels of bac that metabolise dietary plant polysaccharides and increases levels of bile tolerant bac (bacteroides) * iron intake increases bacteroides and decreases bifidobacteria/clostridia * ABs * short term use can induce long term changes * genetics and environment * chronic inflammation

Answer 210

* isolated lymphoid follicles (ILFs) * Peyers patches (only in s intestine) * enterocytes * secrete immunomodulatory cytokines (TGF-beta), chemokines and anti-microbial peptides * goblet cells * secrete mucins, lysozymes, lactoferrin * IELs * effector cells * they include innate lymphocytes/lymphoid cells (ILCs) * they have limited receptor diversity * paneth cells * secrete defensins * M cells * DCs * sample Ag * induce T cell differentiation pathways (steady state=Treg, TH2, inflammatory state=TH1, TH17) * bias B cell isotype switching to IgA * induce mucosal addressin alpha4beta7 (homing receptor) on activated T and B cells

Answer 211

* peristaltic * acid * mucous layer/glycocalyx * enterocytes * barrier with tight junctions and regular replacement * antimicrobial factors * cytokines and chemokines * innate leukocytes * mechanisms for controlled Ag access * M cells, DCs

Answer 212

* LTi= lymphoid tissue inducer cells * recruits DCs, T and B cells * IELs: intraepithelial lymphocytes * involved in host protection, epithelial repair, promotion of tolerogenic DCs, produce IL-22) * subsets of T cells= alpha-beta CD8 some of these express gamma-delta TCR * NK-22 * multiple cytokines including IL-22 * similar to TH17 * IL-22 * enhances antimicrobial defence, epithelial repair and barrier integrity * MAIT= mucosal associated invariant T cells * responds rapidly to bac Ag (riboflavin metabolites) * not really understood * most are CD8 and act on MHC I _like_ cells * invariant NKT cells * proinflamm cytokines * its TCR binds to CD1d (MHC like molecule that binds lipids) * macrophages * express lower levels of TLRs * hyporesponsive to TLR signalling

Answer 213

* peyers patches and mesenteric LNs develop **prenatally** * isolated lymphoid follicles (ILFs) develop **postnatally** * signalling by microbiota via PAMPS on PRR, initiates dev of ILFs * TLR 2, 4 high before birth but then downregulated * TLR 3,7,9 in endosomes * TLR 5 against flagellin is on basolateral surface of enterocyte * microbes enter via M cells--\> further dev * differentiation of NK22 cells, invariant NKT cells, drive tolerogenic DCs, cytokines * B cells in lymphoid tissues produce IgA

Answer 214

* healthy twins attained a normal childhood microbiome * twins with kwashiorkor from a Malawian diet could not maintain a change in gene content when they changed from a malawian diet to a therapeutic diet and back again * mice fed a kwashiorkor microbiome lost weight and their microbiome changed * results indicated * microbiome produced products that lead to inhibition of TCA cycle--\> impaired cellular metab and E production

Answer 215

* obese and non obese ppl have diff gut microbiota * high fat diets are associated with a decrease in diversity of microbiome * T2D has a predictable ultered gut microbiome * ppl with a low microbial diversity have high levels of insulin resistance, serum triglycerides, cholesterol and insulin * in animal models you can transfer obesity by transferring microbiota * microbiota of obese mice show they are rich in genes for CHO metab--\> increased E extraction * obesity= low grade chronic inflammation * inflamm cytokines TNF-alpha, IL-1beta, IL-6, IL17 * increased mast cells, T cells and macrophages * proinflamm signalling desensitises the insulin and leptin receptors * high fat diet fed mice have elevated LPS and intestinal permeability

Answer 216

* IBD= elevated imm response to intestinal microflora * ppl with IBD have lower bac diversity and increased intestinal permeability

Answer 217

* early microbial colonisation is associated with dev of an appropriate gut microbiome and imm system * children who have atopy had higher levels of Clostridia and low levels of Bifidobacteria * Caesarian deliverd infants have a 20% increase in asthma * if mothers are exposed to a range of animals during pregnancy its less likely that their infant will have asthma and allergies * reduced gut microbial diversity in infants--\> later dev of eczema

Answer 218

* alterations in commensals can result in * susceptibility to infection by gastrointestinal pathogens e.g. salmonella * overgrowth of commensals * e.g diarrhoea caused by Candida * Clostridium difficule causing psuedomembranous colitis * gram +, anaerobic, spore forming rod * produces cytotoxins--\> cell death, inflammation and bowel necrosis * treatment= more ABs (metronidazole +/- vancomycin) or bacteriotherapy= rePOOPulate, prebiotics, probiotics * ppl who dev recurrent infections have a reduced diveristy in their microbiom cf those that get single infections

Answer 219

* sleeping MR * BMR * arousal * thermic effect of food * activity

Answer 220

* Doubly labelled water * Oxygen consumption (VO2) * Heart rate based estimation of VO2 * Activity monitors * Population based algorithms

Answer 221

* Adrenaline, thyroid hormones * muscle mass and oxidative capacity * exercise/physical activity levels * non-exercise activity thermogenesis * shivering thermogenesis * brown fat

Answer 222

* CCK, GLP-1, amylin, insulin, leptin--\> decrease appetite * Ghrelin from stomach--\> stimulates hunger

Answer 223

* as you increase your body weight, leptin levels also increase which acts on the brain to decrease food intake

Answer 224

* increased physical activity * reduced E intake, calorie restriction * Pharmacological * appetite suppressants * absorption inhibitors * metabolic activators * Bariatric surgery

Answer 225

* low calorie, low fat diet with minimal varaition * eating breakfast everyday * frequent self monitoring * regular exercise 1hr/day * limiting TV viewing

Answer 226

* malnutrition/starvation * endocrine and GI diseases * infection (TNF-alpha) * cancer cachexia * sustained exercise training * age-related sarcopenia * anorexia nervosa

Answer 227

* where the upper part of the stomach herniates through a hiatus into the thoracic cavity * causes * heartburn * fluid regergitation * oesophageal changes * types * sliding hiatus hernia * common * reflux symptoms * rolling hiatus hernia * not as common * dangerous * gastric vulvolus

Answer 228

* block H1 receptors in the vomiting centre in the medulla * e.g. * Dimenhydrinate * Promethazine

Answer 229

* block M receptors in the vomiting centre in the medulla * e.g. * hyoscine hydrobromide

Answer 230

* most of them go into the CNS except domperidone, therefore they have extrapyramidal SE (e.g. parkinsonisms) * e.g. * Metoclopramide * works in the CNS and gut * D2 antag * stimulates 5-HT4 receptors * increases gastric emptying--\> increase absorption of drugs * used in conditions that have decreased motility * weak anatgonist at 5-HT3 receptors * Prochlorperazine

Answer 231

* has less SE than D2 antagonists * e.g. * ondansetron * SE= constipation, headaches * but effective for nausea, vomiting and chemotherapy

Answer 232

* H1 receptor antagonists * Muscarinic receptor antagonists * D2 receptor antagonists * 5-HT3 receptor antagonists * NK1 receptor antagonists

Answer 233

* bulking agents * faecal softeners and lubricants * osmotic laxatives * stimulant laxatives * others

Answer 234

* hydrophilic colloids/ indigestable vegetable fibre--\> greater faecal water retention--\> greater vol of intestinal contents--\> activates stretch receptors--\>increased normal reflex bowel activity * e.g. * Psyllium

Answer 235

* detergents * enhance mixture of water into faeces * it basically emulsifies the faeces * e.g. * Docusate

Answer 236

* saline laxatives * are slowly absorbed ions which cause osmotic fluid retention--\> colonic stimulation by distension due to increased fluid volume * e.g. * magnesium sulphate (epsom salts)

Answer 237

* irritant laxatives * most potent * precise mode of action is unknown * may stimulate colonic myenteric nerve plexuses, irritant intestinal mucosa or by direct sensory nerve ending irritation * all increase motility * may also reduced net reabsorption of water and electrolytes * e.g. * senna

Answer 238

* opioids * musculotropic antispasmodic * muscarinic receptor antagonists

Answer 239

* act on u-opioid receptors to inhibit the release of Ach * e.g. * Codeine * goes into the CNS * Loperamide * doesn't cross the BBB therefore doesn't have CNS effects and so is not often abused/additive

Answer 240

* defoaming polymers * gastrointestinal decontaminant * carminatives (peppermint, dill, anise, cloves, nutmeg, cinnamon)

Answer 241

* theory of flatulence is that its difficult to pass small air bubbles therefore causing pain and easier to pass larger air bubbles * defoaming polymer--\> coalescence of gas bubbles * smaller air bubbles join together to form large ones that are easier to pass * e.g. * simethicone

Answer 242

Clinical definition * increase serum transaminase enzymes for a period of \<6months duration, in patient with no history of chornic liver disease Pathological definition * it has same pathological changes in the liver as acute viral hepatitis * its a non-specific/ diffuse pattern

Answer 243

* acute viral hepatitis * drug induced liver injury * natural remedies * autoimmune hepatitis * idiopathic

Answer 244

* death of hepatocytes (zone 3 is most vulnerable) * necrosis (of groups of hepatocytes) * apoptosis (single cell death) * regeneration of hepatocytes * absence of fibrosis

Answer 245

* apoptosis * zonal necrosis * bridging necrosis * multi-acinar necrosis

Answer 246

* pan lobular disarray * apoptosis * necrosis of variable extent * aggregates of enlarged macrophages * cholestasis

Answer 247

* resolution with restoration * massive hepatic necrosis * chronic hepatitis

Answer 248

* liver injury caused by a toxic metabolite (NAPQI) which directly injures hepatocytes and causes depletion of glutathione (a natural anti-oxidant) * coagulative necrosis occurs in zone 3 because this is where the enzyme CPY2E1 is located * there is minimal inflammation

Answer 249

* liver * small intestine * in the ER and (mitochondria)

Answer 250

its made up of 2 phases: * phase I detoxification * CYP dependent * catylises a range of rxns: hydroxylation, epoxidation, dealkylation, oxidation * makes toxins more soluble * phase II detoxification * CYP independent * adds a sugar (e.g. glucuronate) to the -OH group of a xenobiotic * makes it even more soluble

Answer 251

* its a monoxygenase * adds a hydroxyl group to a xenobiotic(R) **RH** + NADPH + H + O2 --------\> **ROH** + H2O + NADP+ steps 1. NADPH is oxidised by NADPH cytochrome P450 reductase * releases H+ and 2e 2. H+ and 2 e are used by CYP to reduce one of the two atoms of molecular oxygen--\> water 3. the other oxygen atom is retained in a highly reactive form and used to force a hydroxylation reaction on the substrate

Answer 252

* metabolised by **CYP1A2** * metabolism involves N-3 demethylation and hydroxylation to paraxanthine and 1,3,7-trimethyluric acid

Answer 253

* CYP3A4 * important for drug metab * they are inducible * CYP2D6 * important for polymorphisms * they are polymorphic * ppl deficient in this CYP are poor metabolisers of codeine and therefore get no relief, they also poorly metabolise other drugs--\> higher concentrations of the drugs

Answer 254

* active site * haem prosthetic group * with iron that alternates between Fe2+ and Fe3+ as electrons are donated to O2 * cysteine anchor * forms a ligand to the Fe in haem (the side chain sulphur coordinates to Fe) * hydrophobic protein foot * anchors the enzyme to the ER membrane

Answer 255

* poor metabolisers * homozygous for one deficient allele * or heterozygous for two diff deficient alleles * intermediate metabolisers * heterozygous for one deficient allele * or carry two alleles that cause reduced activity * extensive metabolisers * have two wild type alleles * these people are considered normal * ultra rapid metabolisers * multiple gene copies

Answer 256

* prozac **inhibits** many CYPs (espc CYP2D6) * makes extensive metabolisers resemble poor metabolisers * some drugs **compete** for a particluar CYP for metabolism * TCA have a higher affinity for CYP2D6 which slows down the metab of antipsychotics * grapefruit juice contains furanocoumarin which inhibits CYP3A4 * dioxin induces CYP1A * brussels sprouts, kale, cabbage induces CYP1A2 expression--\> decreased bioavailability of haloperidol (an antipsychotic)

Answer 257

* liver ER preparations called microsomes * supersomes (based on human recombinant enzymes)

Answer 258

* vascular autoregulation (espc in the brain) * formation of cholesterol, steroids and arachidonic acid metabolites (in the mitochondria, espc adrenals)

Answer 259

* normal * mild dysplasia * aka low grade * basal 1/2 atypia * moderate dysplasia * aka high grade * middle 1/3 * severe dysplasia * aka high grade * carcinoma * key feature= invasion * spread via * direct spread * neural * lymphatics * vv

Answer 260

* cell carry a risk of developing into cancer * types * dysplasia * aka intraepithelial neoplasia * carcinoma in situ * at the severe end of dysplasia * they are not invasive yet

Answer 261

* when a benign (orderly neoplasm)--\> malignant neoplasm

Answer 262

* adaptive change in epithelial cell differentiation in response to the microenvironment * response can be * physiological * e.g. cervical transformation zone and HPV infection--\> cervical dysplasia * response to chronic injury * e.g. Barretts oesophagus

Answer 263

* sexually transmitted * \>150 serotypes * low risk types= 6, 11 * high risk types= 16, 18 * episomal viral replication * latent infection * low level of viral replication * integration into host genome * high risk types do this via overexpression of E6 and E7 viral oncogenes

Answer 264

* types 6 and 11 * genital warts * mild squamous dysplasia (CIN1) * aka low grade squamous intraepithelial lesion (LSIL)

Answer 265

* types 16 and 18 * moderate--\> severe squamous dysplasia (CIN2-3) * aka high grade squamous intraepithelial lesion (HSIL) * or can cause squamous cell carcinoma

Answer 266

* E6 binds to p53 and stops its normal function of promoting apoptosis * E7 binds to Rb * no G1/S checkpoint * upregulates p16

Answer 267

* region in the vagina where squamous epithelium meets glandular epithelium * its highly vulnerable to HPV infection and squamous dysplasia

Answer 268

* chronic reflux oesophagitis * repetitive mucosal injury by gastric acid and duodenal contents * exposure to carcinogens in reflux contents * cellular proliferation in attempt to heal * re-epithelialisation by columnar epithelial * (low rate of transformation to the next one, especially if its a short sequence) * (involves genetic events) * oesophageal adenocarcinoma

Answer 269

Diagnositic criteria * columnar lining in oesophageus above gastroeosophageal junction * intestinal metaplasia (presence of goblet glands) identifying the dysplasia * surface maturation of glandular mucosa * architecture of glands * crowding * change in shape and complexity * fland fusion * cytology of proliferating cells * nuclear atypia * loss of polarity * response to inflammation and erosions/ulcers * presence of eosinophils, lymphocytes and oedema

Answer 270

* the kidney

Answer 271

* EPO binds to EPO receptor (member of the Class I cytokine receptor family) * activated EPO R forms a homodimer * phosphorylation by the tyrosin kinase JAK2 (janus kinase 2) * gene transcription

Answer 272

* life cycle= max 120 days * undergoes cyclies of osmotic swelling and shrinkage while travelling through the kidneys and lungs * it deforms while passing through the capillary beds * accumulates damage especially to its membrane * becomes methylated Hb (Fe3+) * doesn't carry O2 as well * therefore goes through the mononuclear phagocyte system/ reticuloendothelial system

Answer 273

* give 51Cr (radioactive substance) in a pulse * it labels all RBCs of all ages * the label is then measured to be removed linearly over 120 days

Answer 274

* white pulp * T, B cells and accessory cells * respond to Ags in the blood * red pulp * system of blood vessels arranged to facilitte removal of old or damaged RBCs * removal is via macrophages

Answer 275

* neuraminic (sialic) acid is lost from glycophorin on membranes surface * oxidative damage products (e.g. Heinz bodies) * more phosphatidylserine flips to the outer side of the membrane

Answer 276

* external attack on red cells * e.g. streptococcus or enterococcus * parasitic haemolysis * e.g. malaria * congenital or genetic factors * e.g. haemolytic disease of the newborn= autoimmune disease where the mothers Abs cross the placenta to attack the foetus

Answer 277

* a plasma protein * binds **haemoglobin** released form RBCs heamolysed at sites remote from the spleen * the CD163 receptor on macrophages recognises the Hb+Hp complex and phagocytoses it

Answer 278

* carries **haem** to the liver

Answer 279

* unconjugated (indirect) hyperbilirubinemia--\> jaundice * increased stercobilin (brown) * increased urobilinogen in the urine (yellow) * cholelithiasis (gall stones form bile acids) * reticulocytosis symptoms= * pallor * fatigue * dizziness * possible hypotension * hemolytic crisis (acute severe hemolysis) * hemoglobinuria= red brown urine

Answer 280

* macrophages breakdown RBCs and release haemoglobin * haemoglobin is broken down into globin and haem * globin is recycled to amino acids * haem (red) is broken down by haem oxygenase to --\> unconjugated biliverdin (green) with the release of iron * biliverdin is reduced--\> bilirubin (yellow) * bilirubin is complexed to albumin to be transported in the blood to the liver * bilirubin is conjugated with glucuronic acid by the enzyme bilirubin UDP glucuronyltransferase--\> conjugated bilirubin (increased water solubility) * enters the biliary system(bile canaliculi) via cMOAT--\> small intestine * bacterial enzymes convert conjugated bilirubin--\> urobilinogen--\> 90% is --\> stercobilin (brown) in faeces * 10% of the urobilinogen enters portal vein to re-enter the hepatocytes--\>9% goes back into the bile canaliculi * 1%--\> blood stream--\> kidney--\> urobilinogen --\>spontanous rxn with O2--\> urobilin (yellow) excreted in urine

Answer 281

* cMOAT= canalicular multispecific organ anion transporter * aka * multidrug resistance associated protein 2 (MRP2) * ATP binding cassette sub-family C member 2 (ABCC2)

Answer 282

* mono- or di-glucuronides

Answer 283

* neonatal hyperbilirubinaemia * bile duct obstruction * severe liver failure with cirrhosis * Crigler-Najjar syndrome * Dubin-Johnson syndrome * Choledocholithiasis (chronic or acute blockage of the bile duct)

Answer 284

* first presentation= reddish because blood is trapped in interstitial tissue * 1-2 days= turns bluish **purple** or even blackish from **deoxy and met-Hb** * 5-10 days= turns **greenish** or yellowish from **biliverdin** * 10-14 days= **yellowish**-brown or light brown from **bilirubin** * \>14 days= fades away

Answer 285

* autosomal recessive disorder * defect in cMOAT * failure to excrete diglucuronide into the bile system * hyperbilirubinaemia due to soluble conjugated bilirubin results * usually asymptomatic * liver shows multiple areas of dark pigments

Answer 286

* autosomal recessive disorder * lack of UGT1A1 (UDP glucuronyltransferase 1) * either inactive (type I) or reduced (type II) * high plasma levels of unconjugated bilirubin--\> jaundice * some exhibit kernicterus= bilirubin encephalopathy and brain damage due to bilirubin toxicity * treatment= phototherapy to reduce bilirubin levels * exposure to blue fluorescent light * Z,Z isomers flips to E,Z or E,E isomers and bilirubin becomes more soluble (internal H bonds change)

Answer 287

* breakdown products of Hb (mostly bilirubin diglucuronide)

Answer 288

* detergent derivatives of cholesterol

Answer 289

* BBB of vv is no barrier to alcohol * EtOH makes nerve membranes become leaky because it disrupts membrane fats--\> impaired signals * its neurotoxic (Wernicke Korsakoff syndrome) * thiamin deficiency * portal hypersion * neurological disturbances * jaundice * altered breath * feminisation * loss of libio * breast cancer risk increases * ascites * hand tremor * hypogonadism/testicular atrophy * hypocoagulability--\> easy bruising * muscle wasting * oedema * brain dehydration --\> shrinking--\> headache, because it interferes with pituitarys function--\> low ADH * alcohol induced liver damage * fatty liver * alcoholic hepatitis * alcoholic cirrhosis

Answer 290

* when withdrawal causes * tremors * anxiety * sweating * vomiting * also when people cannot stop drinking when they realise they should

Answer 291

* its the neurotoxicity that occurs in severe alcoholics * symptoms * eye uncoordinated (nystagmus) * wide step * confusion * hypothermia * amnesia * confabulation (confusing facts)

Answer 292

1. fatty liver * rapid * reversible 2. alcoholic hepatitis * widespread inflammation * fever, jaundice, abdo pain 3. alcoholic cirrhosis * extensive fibrosis that distorts the internal structure of the liver * irreversible

Answer 293

* some undergoes first pass metab in the stomach by alcohol dehydrogenase form gastric mucosa * alcohol absorption is slowed by fats in food * 3 pathways 1. Alcohol dehydrogenase (ADH) * in cytosol * produces acetylaldehyde and NADH * acetylaldehyde is converted to acetate by acetaldehyde dehydrogenase (ALDH) * acetate is then converted to acetyl-CoA which can be used in the TCA cycle to produce E or be stored in fat 2. Microsomal Ethanol Oxidising system (MEOs) * this is induced in chronic drinkers * uses CYP 2E1 (Increased) * CYP4A1 is also increased 3. Catalase * in liver peroxisomes * uses H2O2 as the oxidant

Answer 294

0.015% and women are more affected because alcohol does not distribute into fat

Answer 295

* one hour * its a linear decrease

Answer 296

* ALDH2= mitochondria isoform

Answer 297

* gas chromatography * breath tests (usually gives underestimates)

Answer 298

* No and it may even be low in alcoholics due to liver damage

Answer 299

* 3 drinks in 1 hr to get to the blood alcohol limit

Answer 300

* prevents drug clearance when alcohol is present * promotes drug clearance by elevated CYP 2E1 when alcohol is not present * e.g. you need to increase the protective dose of warfarin when a person is taking alcohol

Answer 301

* damaged cells release inflammatory agents * eicosanoids * cytokines * endotoxins * cells are damaged because * chronic alcohol consumption and dietary neglect--\> diminshed intake of antioxidants (vit A,E,C) * alcohol interferes with the transport of glutathione through membranes--\> depletion of glutathione form mitochondria * glutathione is needed to scavenge the free radicals produced by the mitochondria durin ETC * alcohol metab by the MEOS pathway loads cells with free radicles * alcohol in the gut promotes absorption of iron which becomes a catalyst for free radicle production * acetaldehyde reacts with proteins to form schiffs bases

Answer 302

* its inherited in an autosomal dominant manner * it increases acetaldehyde levels * produces vasodilation with facial flushing * promotes unpleasant feelings when drinking alcohol

Answer 303

* disulfiram * irreversable inhibitor of aldehyde dehydrogenase * --\> acetaldehyde accumulate, tachycardia, flushing, dyspnoea, nausea and vomiting * Naltrexone * opioid receptor antagonist * blocks alcohol induced release of dopamine in nucleus accumbens * decreased pleasurable effects and craving * Nalmefene * mu and alpha opioid receptor antagonist * less hepatotoxic than naltrexone * Dopaminergic drugs * Tiapride * D2 receptor antagonist * Acamprosate * GABA receptor agonist

Answer 304

* can have adverse effects at all time during pregnancy especially during the first trimester * can cause Foetal alcohol syndrome (FAS) * irreversible * its on a spectrum * small heads and eyes * facial malformations etc

Answer 305

* more than 10 standard drinks in one sitting

Answer 306

* lower risk of: * heart attack * diabetes * Alzheimers disease * stroke * increased longevity

Answer 307

Stable joints * congruent articular surfaces * tight capsule with strong ligament * limited ROM mobile joints * stability is dependent on muscles * susceptible to subluxation and dislocation

Answer 308

* articular cartilage * avascular * aneural * fibrous capsule * can be reinforced by stabiliser muscles * it blends with the periosteum * intrinsic ligaments * strengthen the capsule * extrinsic/accessory ligaments * located at some distance away from the join * can be primary stabilisers * synovial membrane * lines all non articular surfaces * vascular * secreates synovial fluid * never located on hyaline cartilage!

Answer 309

* labrum * tendon * fat pad * discs and menisci * bursae * ligaments

Answer 310

* joints of the clavicle * sternoclavicular joint * acromioclavicular joint * glenohumeral joint * scapulo-thoracic joint

Answer 311

* triangular bone * thin bone with smooth surface therefore muscles attach via muscle fibres not tendons * spine divides sections: supraspinous fossa and infraspinous fossa * glenoid fossa

Answer 312

* orienates shoulder laterally from increased ROM (2:1 ratio instead of normal 1:2 ratio) * allows scapulo-humeral rhythm * curved bone * attachments for costococlavicular ligament and coracoclavicular ligament * joints * sternoclavicular * acromioclavicular

Answer 313

* intra-articular disc * very stong capsule * costoclavicular/accessory ligament

Answer 314

* persistence of liver injury with raised serum aminotransferase levels of \> 6months * note: not all ppl with elevated liver enzymes have chronic hepatitis

Answer 315

* chronic HBV, HCV (most common cause) * autoimmune hepatitis * drugs

Answer 316

* interface hepatitis * periportal hepatocellular injury and lymphoplasmocytic inflammation * death of hepatocytes is mainly via apoptosis but necrosis can also occur * fibrosis * via heaptic stellate cells NOT portal fibroblasts * cytokine induce hepatic stellate cell activation--\> conversion to fibrogenic myofibroblasts * has stages 1,2,3,4

Answer 317

* both involve T cells * acute * pan lobular hepatocellular injury * no fibrosis * chronic * inflammation in portal tracts and periportal liver tissue associated with injury of periportal hepatocytes * lymphocytes and plasma cells * fibrosis can occur--\> cirrhosis

Answer 318

* damage from **acetylaldehyde** * **oxidative stress** * impaired CHO and fat metabolism * collagen synthesis * genetic susceptibility * fatty changed= **steatosis** * **alcoholic steatohepatitis** * **ASH** * =fat and damage * if severe will can acute alcoholic hepatitis * damage= **swelling** and Mallory Denk bodies * **Mallroy Denk bodies** * collapse of cytoskeleton * attracts neutrophils * **progressive fibrosis--\> cirrhosis--\> HCC** * **'**chicken wire fibrosis'

Answer 319

* **fatty change** with or without * **non-alcoholic steatohepatitis (NASH)** * ****MD bodies aren't as common * not severe * may not even be present * **progressive fibrosis--\>cirrhosis--\>HCC** * doesn't really look different to alcoholic liver disease under the microscope. The real difference is in the clinical Hx * collagen fibres= more delicate

Answer 320

* between lateral 1/3 and medial 2/3 * at the areas of maximum curvature

Answer 321

* plane synovial joint * articular surfaces in sagittal plane * weak capsule * main stabiliser= coracoclavicular ligament (2 parts) * trapezoid part * conoid part

Answer 322

* intra-articular disc * strong capsule * very stable joint * costoclavicular(accessory) ligament

Answer 323

* acromioclavicular subluxation

Answer 324

* layer 1 * bones and articular surfaces * synovial ball and socket joint * disproprotionate size of humeral head to shallow glenoid fossa * unstable joint * layer 2 * labrum * deepens socket * has attachment superiorly for long head of biceps and glenohumeral ligaments * layer 3 * capsule * allows ROM in 3 planes * attaches to anatomical neck above and surgical neck below * reinforced by intrinsic ligaments * deficiencies anteriorly for long head of biceps and bursa * layer 4 * tendons * rotator cuff * originate form scapula and insert into capsule * mainly act as stabilisers (pulls humeral head towards glenoid and compresses it) but also prime movers * layer 5 * coraco-acromial (accessory) ligament and sub-acromial bursa

Answer 325

* endangers the axillary nerve * common in elderly

Answer 326

* endangers the radial nerve

Answer 327

* endangers the median nerve and the brachial artery

Answer 328

* when the glenohumeral joint capsule contracts

Answer 329

* the humerus is susceptible to slide upwards with the pull of deltoid * can lead to entrapment/impingement of supraspinatous

Answer 330

* the coracoacromial ligament between the acromion and coracoid

Answer 331

* it tears and then calcifies

Answer 332

* anterior is most common due to force applied to abducted and externally rotated arm * posterior is less common especially during electric shock and epileptic fits * difficult to determine from an AP film * a lateral view parallel to the plane of scapula shows it better

Answer 333

* axillary nerve in quadrangular space * endangered by inferior disolaction * supplies deltoid and overlying skin

Answer 334

* collateral ligaments * medial/ ulnar * lateral/radial * annular ligaments * lateral collateral ligament and annular ligament permits pronation and supination

Answer 335

* maximum stability is in extension because the ligaments are taut

Answer 336

* =carrying angle * aka cubitus valgus * if it is increased it can result in friction on ulnar nerve

Answer 337

* enables the 2 radioulnar joints to act as 1

Answer 338

* annular ligament is weak especially in children * upward pull on extended arm may pull radial head out of annular ligament

Answer 339

* posterior dislocation * results in a fracture of the coronoid process

Answer 340

* common in children * stretch and spasm of brachial artery * can lead to ischaemia (Volkmann's) of the forearm musculature

Answer 341

* medial epicondyle fracture * the ulnar nerve is susceptible to injury * lateral epicondyle injury * aka lateral epicondylitis * =tendinitis of wrist extensor muscle in activities involving extension, pronation and wrist flexion

Answer 342

* FAP (Familial adenomatous polyposis) * Lynch syndrome

Answer 343

* 100% risk of cancer * due to chromosomal instability * mutation in APC gene * decreased cell adhesion and increased cell proliferation * lots of polyps

Answer 344

* non polyposis * 70-80% risk of cancer * due to microsatellite instability * mutation in DNA mistmatch repair gene * early onset cancer * few polyps * more common than FAP

Answer 345

mnemonic: SOME LOVERS TRY POSITIONS THAT THEY CAN'T HANDLE

Answer 346

* synovial ellipsoid joint * articular surfaces concave in 2 directions * the ulna does not articular at the wrist * flexion is \> than extension * ulnar deviation \> radial deviation

Answer 347

* funcitonal rather than anatomic joint * no single joint capsule- each bone forms a separate unit * extension \> than flexion * radial deviation \> ulnar

Answer 348

* the distal radius with the clavicle * called a Colles fracture * occurs especially in the elderly

Answer 349

* the scaphoid * affects blood supply * causes avascular necrosis of lunate bone

Answer 350

* lunate is most commonly subluxed secondary to the radio-schaphoid-lunate injury

Answer 351

* fracture base of 1st metacarpal (Bennett's) and neck of 5th metacarpal (Boxer's)

Answer 352

* all are synovial joints * carpometacarpal joint of the thumb is a saddle joint * metacarpals II-V are linked by deep transverse metacarpal ligament * joints II-III are immobile * IV and V are hinge joints

Answer 353

* flexion and extension * abduction and adduction

Answer 354

* flexion and extension only

Answer 355

* all are condyloid joints * contains a volar plate/fibrocartilaginous plate * expands SA for articulation

Answer 356

* called a Swan neck deformity * hyperextension at the site of the injury * compensatory flexion at the distal end

Answer 357

* called a Boutonniere deformity * flexion at the site of injury * compensatory hyperextension distal to injury

Answer 358

* add bicarbonate * diultes and increases the alkalinity of the bile

Answer 359

* fats become indigestible and are instead excreted in faeces that lack their characteristic brown colour and are white or grey and greasy

Answer 360

* steroid structures with a carboxylic acid group that is commonly linked to glycine or taurine to increase its solubility

Answer 361

* cholic acid * deoxycholic acid * chenodeoxycholic acid

Answer 362

* the recovery process where 95% of the salts secreted in bile are reabsorbed in the terminal ileum

Answer 363

* secretin * cholecystokinin

Answer 364

* indirect bilirubin

Answer 365

* prehepatic * haemolysis (haemolytic anaemia) * ineffective erythropoiesis * intrahepatic * drugs * intrahepatic obstruction * Gilberts syndrome * Dubin-Johnson syndrome * Cringler-Najiar syndrome * post hepatic * gall stones * carcinoma of the pancreas * neonatal jaundice

Answer 366

* G-6-PD deficiency

Answer 367

* caused by * increased haem catabolism * immaturity of the liver in bilirubin conjugation and excretion * haemolytic disorders * glucose-6-phosphate dehydrogenase deficiency * most common cause * confers resistance to malaria * aka favism * death because you cant produce glutatione and therefore cannot protect agaist oxidative stress * birth trauma * premature birth * breast feeding = causes benign jaundice * becomes a problem when babies switch from foetal haemoglobin to adult haemoglobin * treated by phototherapy (blue light)

Answer 368

* disease where an infant is unable to metabolism milk * unmetabolised milk sugars therefore build up and damage the liver, eyes, kidneys and brain * cataract formation occurs because it is due to osmotic effect of galacitol formed by aldehyde reductase

Answer 369

* aggressive form of chronic hepatitis * presence of auto-antibodies

Answer 370

* type 1 * most common * occurs in adult women * associated with anti-smooth muscle antibodies * type 2 * occurs in children and teenagers * associated with anti-liver kidney microsome

Answer 371

* **severe early phase** * destruction of liver cells * presents as acute hepatitis * fibrosis develops **rapidly** in areas of collapse * lots of **plasma cells**

Answer 372

* **end stage to many chronic liver diseases** * **conversion of liver--\> nodules of regenerating hepatocytes surrounded by bands of fibrous tissue** * **diffuse** * vascular shunting occurs * cf to chronic hepatitis, cirrhosis develops slowly * its **pattern can vary** * causes * ALD * NASH * chronic HBV and HCV * autoimmune hepatitis * chronic biliary disease * metabolic * drugs * can lead to HCC * pathogenesis of cirrhosis * scars and fibrous septa develop **in areas where hepatocytes have dropped out** due to inflammation injury to portal veins * cirrhosis is driven by **parencyma extinction caused by vascular inflammation, thrombosis and vascular occlusion** * **NOT due to direct effect of injury**

Answer 373

* ascites * porto-systemic anastomoses * congestive splenomegaly * hepatic encephalopathy

Answer 374

* obstruction to flow * cirrhosis= most common cause

Answer 375

* exponential curve * amount of drug in body falls exponentially with time * there is a rapid rise in concentration initially * drug concentration falls more slowly at lower concentrations

Answer 376

* rate of accumulation decreases as concentration increases * once infusion is stopped, only elimination occurs * the peak is not as high as for IV bolus * good for drugs that have a narrow/small T.I

Answer 377

* continued infusion until equilibrium is reached * at steady state rate of infusion= rate of elimination * concentration of steady state is proportional to infusion rate * therefore easy to dial up concentration

Answer 378

* will reach the same steady state as a constant rate * time to reach steady state * 30% in 1 t1/2 * 90% in 4 t1/2 * 99% in 7 t1/2 * therefore you need a loading dose

Answer 379

* conveinent * absorbed from the GIT especially from the small intestine * superfolded * villi and microvili * increases SA * can undergo 1st pass hepatic metabolism (not all drugs undergo this) * peak isnt as high as with IV because there is some elimination during absorption

Answer 380

* **proportion of active drug which enters systemic circulation** * **depends on route of administion** * bioavailability=absolute bioavailability of the drug for oral or subcutaneous drugs not IV admin drugs * calculated by the **area under the curve**

Answer 381

* unusual drug behaviour * interpatient variability

Answer 382

* low bioavailability * **any variability in doses will have greater consequences** * therefore you need to give drug in another way * drug reservoirs * **sites where drug accumulates** * can prolong action or can quickly terminate action or can lead to slow distribution * e.g. * plasma proteins * cells * fat * saturable elimination processes * **zero order elimination** * at high concentrations. elimination enzyme is saturated and therefore elimination is constant * at lower concentrations, elimination is no longer saturated and therefore there is now exponential elimination * **only becomes an issue in multiple dosing regimes** * because steady state is never reached * increases in doses--\> disproportionate increases in concentration * slow distribution * when initial distribution is limited * therefore **peak concentration is higher than expected** * a problem if T.I is low

Answer 383

* age * renal excretion problems * metabolism problems * genetics * polymorphisms of metabolising enzymes * fast vs slow metabolisers * idiosyncratic rxns * disease * diseases affecting absorption * e.g. gastric stasis in migraine * diseases affecting metabolism * e.g. liver cirrhosis * diseases affecting excretion * e.g. renal failure * drug - drug interactions * displacement from plasma protein binding site * inhibition of CYP450 * change in drug excretion

Answer 384

* digoxin * phenytoin

Answer 385

AST \> ALT s=short for acute disorders

Answer 386

ALT \> AST L=long for chronic/resolving

Answer 387

ALP GGT * extra-hepatic biliary obstruction * GGT and ALP are massively increased * intra-hepatic biliary obstruction * GGT and ALP and increased slightly

Gastrointestinal Flashcards

(442 cards)