week 3 Flashcards

1
Q

endocrine function of pancreas

A

islets of langerhans secrete insulin, glucagon, somatostatin, polypeptides

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2
Q

exocrine function of pancreas

A

secretory acini
role in digestion and absorption
pancreatic juice secreted - enzymes, sodium bicarbonate
enzymes include amylase, lipase, trypsin, chymptrypsin, esterases

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3
Q

acute pancreatitis signs and symptoms

A

sudden onset of abdo pain, nausea, vomiting, fever, hypotension, shock, multi-organ failure
increase in amylase, lipase and urea
decrease in albumin and calcium

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4
Q

acute pancreatitis causes

A
exact pathogenesis uncertain - duct obstruction, acinar cell injury, hereditary
gallstones
alcohol
metabolic: hypertriglyceridaemia, hypercalcaemia
drugs
trauma
infections eg mumps
ampullary or pancreatic tumours
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5
Q

what is chronic pancreatitis

A

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

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6
Q

signs and symptoms of chronic pancreatitis

A

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

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7
Q

tests of pancreatic damage and results

A

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

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8
Q

faceal tests

A

faecal chymotrypsin and elastase - low values indicate pancreatic insufficiency

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9
Q

function of chymotrypsin and elastase

A

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

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10
Q

what is coeliac disease

A

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

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11
Q

who should be tested for coeliac disease

A

those with symptoms such as diarrhoea, dyspepsia, chronic abdo pain, vomiting, chronic constipation, anorexia, weight losee

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12
Q

how do you test for coeliac disease

A

the patient must be on gluten-containing diet
serology - IgA deficiency
duodenal biopsy - histology, immunohistochemistry, human leucocyte antigen, small bowel imaging

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13
Q

how do you manage coeliac disease

A

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

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14
Q

what are the main complications of coeliac disease

A

infection - howell-jolly body and target cells

functional hyposplenism

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15
Q

pathophysiology of coeliac disease

A

proteases cannot digest gluten

gluten peptides are deamminated by TTG

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16
Q

pathophysiology of coeliac disease

A

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

17
Q

enteropathy associated t-cell lymphoma

A

type 1 is strongly associated with coeliac and HLA-DQ2

18
Q

absorption of iron

A

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

19
Q

transport of iron

A

transferrin transports iron in plasma
it is a glycoprotein synthesised in hepatocytes - has 2 iron binding domains
30% saturated with Fe

20
Q

storage and recycling of iron

A

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

21
Q

regulation of iron metabolism

A

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

22
Q

hereditary haemochromatosis

A

increase in iron, ferrin and transferrin saturation
abnormalities of the HFE gene - reduces hepcidin production
increased GI iron absorption and increased RES iron release

23
Q

RES iron release

A

RES macrophages acquire iron from effete RBCs and the iron is sorted as ferritin or haemosiderin
release is controlled by ferroportin and hepcidin

24
Q

iron deficiency anaemia RBCs

A

small and pale

not enough haemoglobin

25
Q

role of hepcidin in iron metabolism

A

it reduces the levels of iron in plasma
hepcidin binds ferroportin and degrades it - reduces GI iron absorption and reduces macrophage iron release from the RES
it is synthesised in the liver
hepcidin loss causes increased GI iron absorption