Case 10 SBA Flashcards
Vertical quadrant line
midline from xiphoid process to pubic symphysis
Horizontal quadrant line
through the umbilicus
RUQ contents
right lobe of the liver, gallbladder, pylorus of the stomach, first 3 parts of the duodenum, head of the pancreas, right kidney and adrenal gland, distal ascending colon, hepatic flexure of colon, and right half of the transverse colon
LUQ contents
left lobe of the liver, spleen, stomach, jejunum, proximal ileum, body and tail of the pancreas, left kidney and adrenal gland, left half of the transverse colon, splenic flexure of the colon, superior part of the descending colon
RLQ contents
majority of the ileum, caecum, vermiform appendix, proximal ascending colon, right ureter, part of the bladder, uterus, ovary and uterine tube (female) or ductus deferens (male).
LLQ contents
distal descending colon, sigmoid colon, left ureter, part of the bladder, uterus, ovary and uterine tube (female) or ductus deferens (male)
Vertical division lines
two lines between the midclavicular and mid-inguinal point on each side
Superior horizontal line
subcostal or transpyloric plane (L1)
Inferior horizontal line
line between tubercles of the iliac crest on each side (intertubercular plane)
Right hypochondrium
top right. Liver, gallbladder, small intestine, ascending colon, transverse colon, right kidney.
Epigastric region
top middle. Oesophagus, stomach, liver, spleen, pancreas, small intestine, transverse colon, parts of the left and right kidney, adrenal glands and ureters.
Left hypochondrium
top left. Stomach, part of the left lobe of the liver, left kidney, spleen, tail of the pancreas, parts of the small intestine, transverse colon, descending colon
Right flank/lumbar
middle right. Part of the liver, gallbladder, small intestine, ascending colon, right kidney.
Umbilical region
middle middle. Stomach, pancreas, small intestine, transverse colon, parts of the kidneys and ureters, cisterna chyli.
Left flank/lumbar
middle left. Small intestine, part of the descending colon, part of the left kidney.
Right iliac fossa/groin
bottom right. Small intestine, appendix, caecum, ascending colon, right ovary and uterine tube (female), ductus deferens (male).
Hypogastric/suprapubic
bottom middle. Small intestine, sigmoid colon, rectum, urinary bladder, right and left ureters, uterus (female), ovaries and uterine tubes (female), ductus deferens, seminal vesicle and prostate (male).
Left iliac fossa/groin
bottom left. Small intestine, descending colon, sigmoid colon, left ovary and uterine tube (female), ductus deferens (male).
What are gallstones made of?
Components of bile
What three ways can gallstones be formed?
cholesterol supersaturation, mucin acting as a nidus for crystal formation, or changes in gallbladder motility
Cholesterol stones
white stones made from cholesterol, 60-80% of gallstones, 10-15% of UK adults will have them at some point in their lives. Occur as solitary stones, in pairs, or as multiple mulberry stones. Associated with high cholesterol, pregnancy, diabetes, and the oral contraceptive pill.
Pigment stones
small, black, irregular, multiple, gritty, and fragile. Associated with increase haemolysis. Results in increased unconjugated bilirubin in circulation and in bile β in bile it complexes with calcium and gives calcium bilirubinate precipitates
Mixed stones
contain cholesterol, bilirubin, calcium, and other components. Typically arise secondary to infection or after biliary surgery. Damaged hepatocytes and bacteria release beta glucuronidase which hydrolyses conjugated bilirubin. This causes stones to form, as the now unconjugated bilirubin is insoluble.
Describe the role of the gallbladder
reservoir for bile with a 50ml capacity. It stores and concentrates bile and also secretes mucus
What is bile made of?
water, bilirubin (from RBC breakdown), bile salts (taurocholic acid, glycocholic acid, and deoxycholic acid from cholesterol metabolism), bile acids, cholesterol, phospholipids, proteins, amino acids, ions, minerals, and mucin
What are the functions of bile?
fat digestion (emulsification, enzyme action, micelle formation), absorption of fat-soluble vitamins, excretion of toxins, bile, and cholesterol, and to protect intestinal mucosa.
Describe the mechanism of enterohepatic circulation for bile salts
Cholesterol broken down into primary bile acids. These move into the duct and can be stored in the gallbladder. About half go into the small intestine until they hit the ileum. Bacteria in the terminal ileum metabolise the acids into secondary bile acids. A small proportion of the secondary acids move through the rest of the digestive system, but most gets reabsorbed by the blood stream (portal system). Back in the liver, the secondary acids become conjugated with amino acids to form bile salts. The circulation repeats and the salts are recylced.
Primary bile acids
Cholic acid and chenodeoxycholic acid
Secondary bile acids
Deoxycholic acid and lithocholic acid
Bile salts examples
Taurocholic acid and glycocholic acid
Describe the control of the gallbladder after a meal
Fatty meal consumed β> moves through the duodenum and stimulates enteroendocrine cells to release cholecystokinin (hormone, CCK). CCK travels to gallbladder and liver and stimulates them to release bile β squeezes gallbladder and concentrated bile squeezed into intestines. Bile salts break down the fat - hydrophobic portion binds to the fat and the hydrophilic portion (amino acid) exposed to the liquid environment π‘ͺ formation of micelles that can be broken down by pancreatic enzymes.
Other functions of CCK
relaxation of the hepatopancreatic sphincter (of Oddi) which allows bile and pancreatic secretions to enter into the descending duodenum
Action of secretin in the GI tract
secreted in response to acid in the duodenum, stimulates duct cells to secrete bicarbonate and water and also stimulates hepatic bile secretion.
Vagus nerve control of gallbladder/liver
reinforces contraction of the gallbladder, relaxation of the hepatopancreatic sphincter of Oddi, and hepatic bile secretion.
Define major histocompatibility complex
Cell surface protein complexes that enable T lymphocytes to identify non-self/foreign invaders in T cell training
Describe MHC I
present on the membrane of all nucleated cells, differentiates self from non-self, recognised by CD8+ T cells β cytotoxic T-cells.
Describe MHC II
only present on the membrane of antigen presenting cells, immune cell communication and adaptive immunity activation, recognised by CD4+ T cells β helper T cells
Isograft
transplantation between genetically identical individuals
Xenograft
transplantation between different species, used routinely in oncology research
Autograft
transplantation from one part of the body to another part of the body within the same individual.
Allograft
transplantation between non-genetically identical members of the same species. Conventional transplant surgery. Requires blood group, tissue type, and size organ matching.
Indirect allorecognition rejection
Antigen presenting cells originate from the host immune system
Direct allorecognition rejection
Antigen presenting cells originate from the donor graft tissue
How is rejection in bone marrow transplants different?
potential for transplanted T cells to perceive the entire recipients body as foreign β this is known as graft versus host disease. To avoid this, bone marrow transplants require very accurate tissue matching (HLA gene matching).
Describe tissue matching and why it is important
Tissue matching looks at pairing individuals with similar HLA genes and hence similar MHC complexes. Tissue matching is fundamentally important to prevent inappropriate T cell activation in allograft transplantation β transplanted tissue that is not genetically identical to the host will likely express different MHCI which can activate T cells.
Allogeneic MHC complex
Genetically different MHC complexes between host and donor - present on surface of donor tissue and will be perceived as foreign by host T cells
MHC I rejection mechanism
MHCI bind βAlloantigensβ β peptides generated from degradation of cytosolic proteins within non-host cells ο TCR receptors recognise the proteins that make up the allogenic MHCI as not self ο cytotoxic T cells launch and immune response and degranulate ο apoptosis is mediated by cytotoxins.
Indirect allorecognition rejection mechanism
host APC cells take up and present donor alloantigens on their MHCII complexes β> in the lymph node, T helper cells recognise and bind donor alloantigen/MHCII complexes presented on the host APCs and produce cytokines to stimulate B cell differentiation β> differentiated plasma cells undergo antigenic switch β switch from making IgM to IgG specific to donor alloantigens β> opsonisation β IgG antibodies bind donor alloantigen/MHCI complexes resulting in antibody mediated injury via activation and recruitment of leukocytes.
Direct allorecognition rejection mechanism
donor APC express both allogeneic MHC I and II on their surface β> donor APCs take up and present alloantigens on MHCII from damaged donor tissue whilst also presenting self-antigens on MHCI β> host helper T cells recognise and bind donor allogeneic MHC II presented on donor APC whilst host cytotoxic T cells recognise and bind donor allogeneic MHC I presented on donor APC β> T helper cells generate cytokines and cooperatively activate cytotoxic T cells β> cytotoxic T cells can recognise and destroy donor graft tissue expressing allogeneic MHC I β> T helper cells bound to donor allogeneic MHC II stimulate and activate B cells to produce IgG specific to donor MHC I which ultimately leads to antibody-mediated injury to graft tissue.
Functions of the liver
Metabolism of carbs, lipids, proteins, amino acids. Storage of vitamins A, D, E, K and iron. Detoxification, bile formation, bilirubin metabolism
Fat metabolism
oxidation of fatty acids.
Fatty acids then split by beta oxidation into two-carbon acetyl radicals that form acetyl-CoA which enters the citric acid cycle. 80% cholesterol is converted into bile salts, the rest is carried by lipoproteins in the blood to cells or adipose tissue to be stored
Metabolism of proteins
deamination of amino acids, formation of urea, formation of plasma proteins, interconversion of various amino acids and synthesis of other compounds from amino acids
Haemoglobin/bilirubin metabolism
After RBCs complete their life cycle, they are broken down in the spleen and liver β haemoglobin is released and broken into haem and globin β globin broken into amino acids and haem broken into iron and biliverdin (catalysed by haem oxygenase) β biliverdin converted into unconjugated yellow bilirubin by biliverdin reductase β albumin required for transport to liver β becomes conjugated in liver with glucuronic acid β into duodenum and colon β converted into urobilinogen and stercobilinogen (10-15% absorbed into blood β can reach kidney to be excreted as urobilin or liver via enterohepatic circulation).
Phase 1 biotransformation in liver ( metabolism)
catalysed by CPY450 mixed function oxygenase system in the endoplasmic reticulum, may include oxidation, reduction, hydrolysis, and hydroxylation
Phase 2 biotransformation in the liver (conjugation)
increases the negative charge of substances making them more hydrophilic, may include glucuronidation, sulphation, methylation, acetylation, and glutathione transfer. Most commonly catalysed by UDP-glucuronyl transferase producing glucuronide derivatives
Phase three biotransformation in the liver (secretion)
involves transport of drug out of hepatocyte into the canaliculi and is mediated by the ABC super family of transport proteins
