week 3 Flashcards
endocrine function of pancreas
islets of langerhans secrete insulin, glucagon, somatostatin, polypeptides
exocrine function of pancreas
secretory acini
role in digestion and absorption
pancreatic juice secreted - enzymes, sodium bicarbonate
enzymes include amylase, lipase, trypsin, chymptrypsin, esterases
acute pancreatitis signs and symptoms
sudden onset of abdo pain, nausea, vomiting, fever, hypotension, shock, multi-organ failure
increase in amylase, lipase and urea
decrease in albumin and calcium
acute pancreatitis causes
exact pathogenesis uncertain - duct obstruction, acinar cell injury, hereditary gallstones alcohol metabolic: hypertriglyceridaemia, hypercalcaemia drugs trauma infections eg mumps ampullary or pancreatic tumours
what is chronic pancreatitis
irreversible pancreatic damage leading to destruction of both exocrine and endocrine function
often secondary to repeated acute attacks or alcohol
other causes are hypercalcaemia, idiopathic, tropical
signs and symptoms of chronic pancreatitis
recurrent abdo pain radiating to back
diabetes mellitus due to loss of islet cells
weight loss and steatorrhoea due to malabsorption - 90% of acinar tissue has to be lost before symptoms of malabsorption
tests of pancreatic damage and results
serum amylase - blood amylase is low and constant but greatly increase in acute pancreatitis or salivary gland inflammation - rises within 5-8 hours of onset and normalises by day 4 - low specificity
urine amylase - can help exclude macroamylasaemia when serum amylase increases but urine amylase decreases
serum lipase - rises within 4-8 hours of onset of symptoms, peaks at 24, hours and normalises within 8-14 days - higher sensitivity and specificity
faceal tests
faecal chymotrypsin and elastase - low values indicate pancreatic insufficiency
function of chymotrypsin and elastase
c - acts on peptide bonds in which carboxyl group is provided by tyrosine and phenylalanine
e - broad specificity on attacking bonds nect to small amino acids
what is coeliac disease
a common chronic, immune-mediated enteropathy that is triggered and maintained by ingestion of gluten in genetically predisposed individuals
various degrees of intestinal inflammation ranging from intraepithelial lymphocytes to severe infiltration and total villous atrophy coupled with crypt hyperplasia
who should be tested for coeliac disease
those with symptoms such as diarrhoea, dyspepsia, chronic abdo pain, vomiting, chronic constipation, anorexia, weight losee
how do you test for coeliac disease
the patient must be on gluten-containing diet
serology - IgA deficiency
duodenal biopsy - histology, immunohistochemistry, human leucocyte antigen, small bowel imaging
how do you manage coeliac disease
gluten free diet - dietician review, GP FP10 prescription
nutritional assessment
bone health
vaccination - pneumococcus, menigococcus
follow up with dietician until antibodies normal and diet established
what are the main complications of coeliac disease
infection - howell-jolly body and target cells
functional hyposplenism
pathophysiology of coeliac disease
proteases cannot digest gluten
gluten peptides are deamminated by TTG
pathophysiology of coeliac disease
proteases cannot digest gluten
gluten peptides are deamminated by tTG and presented to APCs
if you have HLA DQ2/8 then APCs can provoke t and b cells to produce anti-gluten antibodies
these induce cytokine cascades which drives the inflammation process
enteropathy associated t-cell lymphoma
type 1 is strongly associated with coeliac and HLA-DQ2
absorption of iron
predominantly in duodenum
haem iron easily absorbed into enterocytes
non-haem iron released from food by acid digestion and proteolytic enzymes in stomach
non haem iron must be reduced from ferric to ferrous state by duodenal cytochrome b1 - influenced by vitamin c
iron is taken into enterocyte through the divalent metal transporter 1 (DMT1)
exported from enterocyte to the circulating plasma transferrin through ferroprotein (transmembrane protein) and the circulating hormone hepcidin
transport of iron
transferrin transports iron in plasma
it is a glycoprotein synthesised in hepatocytes - has 2 iron binding domains
30% saturated with Fe
storage and recycling of iron
effete RBCs are removed by the macrophages of the reticuloendothellial system
RES stores around 500mg of iron
it is stored in ferritin/haemosiderin
releases iron to transferrin in plasma
Tf-iron taken up via Tf receptors on erythroblasts, hepatocytes
regulation of iron metabolism
regulation of dietary iron absorption is the single physiological mechanism responsible for maintaining our iron balance
there is no excretory mechanism for iron
interaction between ferroprotin and hepcidin is the most important regulator of GI iron absorption and RES iron release
hereditary haemochromatosis
increase in iron, ferrin and transferrin saturation
abnormalities of the HFE gene - reduces hepcidin production
increased GI iron absorption and increased RES iron release
RES iron release
RES macrophages acquire iron from effete RBCs and the iron is sorted as ferritin or haemosiderin
release is controlled by ferroportin and hepcidin
iron deficiency anaemia RBCs
small and pale
not enough haemoglobin
