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57 Cards in this Set

  • Front
  • Back
3 small bowel diseases which show dysregulation in their immune system
IBD
coeliac
primary immune def
name some mucosal tissues of the human body
GI tract (salivary gglands- anal canal), resp tract, uro-genital tract, mammary glands
GI tract (salivary gglands- anal canal), resp tract, uro-genital tract, mammary glands
name some secondary lymphoid tissues
remember: peyer's patches in small intestine (ileum)
remember: peyer's patches in small intestine (ileum)
what specialised epithelial cells are present in Peyer-s patches (ileum)
- what are their characteristics
what are the function of M cells at the epithelial surfaces of Peyer's patches?
- by what transport mechanism
- what happen's on the lamina propria side?
M cells in close proximity to underlying immune cells.
TRANSPORT ANTIGENS--->lamina propria side: co-stimulatory signals
M cells in close proximity to underlying immune cells.
TRANSPORT ANTIGENS--->lamina propria side: co-stimulatory signals
apart from M cells in Peyer's patches of the ileum, what other cells in the epithelium are important for the gut's immune defence
& CD8 killer T cells
& CD8 killer T cells
villi (in addition to peyer's patches) also contain immune cells.
- which are in the lamina propria
CD4, mac, mast, dendritic, plasma cells
CD4, mac, mast, dendritic, plasma cells
how are activated effector T cells sent to their destined place in the lamina propria of the small intestine?
T cells 'homed' to peyer's patched → dendritic cells present antigen → T cells activated → lymph →blood → appropriate chemokines & receptors attract effector T cells to gut.
which receptor do activated effector cells bind to on the endothelium of gut capillaries to enter the villi where they will act
MadCAM-1
which Ig predominates in the humoral intestinal response produced by plasma B cells
- role
80% IgA- AGGLUTINATION & NEUTRALISATION at mucosal sites (also at other mucosal tissues)
80% IgA- AGGLUTINATION & NEUTRALISATION at mucosal sites (also at other mucosal tissues)
Intraepithelial Lymphocytes (IELs): T cell (CD8) expression of which integrin anchors them in the epithelium
αE:β7
αE:β7
what cell type are the majority of IELs? (intraepithelial lymphocytes)
- how do they respond to epithelial cell infection
CD8+ Killer T cells
- kill infected cell via perforin/granzyme & Fas-dependent pathways
CD8+ Killer T cells
- kill infected cell via perforin/granzyme & Fas-dependent pathways
in mucosal hyperresponsiveness, T cells show a higher level of activation & a stronger response where there shouldn't be.
- what molecules are absent to prevent dendritic and T cell maturation?
chemokines
IgA def is a primary immunodef, what disease does is predispose to
coeliac's disease
food allergy demonstrates what type of hypersensitivty
- cells involved?
- common symptoms
IMMEDIATE type 1 IgE-mediated
cross-link on MAST cells

- vomiting (intestinal contraction)
- diarrhoea
- puritis (itching_, urticaria (itching), anaphylaxis (rare) : from wide haematogenous dissemination
which enzyme is present in coeliac's disease that modifies gluten so it can be presented to CD4 T cells (MHCII) causing an autoimmune response?

- what type of hypersensitivity reaction does it show
tTG (tissue transglutaminse)
can be used for dx

- DELAYED type 4 hypersensitivity: Tcells & macrophages
how to dx (Ix's) for coeliac's disease
BIOPSY
serology: IgA & tTG
2 types of autoimmune inflammatory hepatobiliary cirrhosis
autoimmune hepatitis
primary biliary cirrhosis
(? primary sclerosing cholangitis- suggested)
autoimmune hepatitis is a type of autoimmune inflammatory hepatobiliary cirrhosis...which shows loss tolerance against liver tissues
- which 3 serum antibodies can be detected on Ix
antibodies to:
- nuclear antigens (ANA)
- smooth muscle (ASM)
- liver kidney microsomala antigens (LKM1)
PBC (primary biliary cirrhosis) is a type of autoimmune inflammatory hepatobiliary cirrhosis...showing chronic cholestatic LIVER disease with small & medium INTRAhepatic duct destruction.
- which serum antibody can be detected in high concs?
IgG AMA (antimitochondrial ab's) 98% - M2 subtype
only therapy for PBC
UDCA (ursodeoxycholic acid)
where's the control centre for energy homeostasis ( integrates neural & hormonal)
hypothalamus
what controls short-term satiation
PEPTIDES produced in the STOMACH & GI tract
what controls long-term body weight
HORMONES
which peptides controlling short-term satiation is released from the I-cells of the duodenum & jejunum
- in response to what
- effect
CCK in response to FAT & PROTEIN
seonsory --> hindbrain
which2 peptides controlling short-term satiation is released from the L-cells of the GI tract
- in response to what
- effect
1) PeptideYY (PYY) AFTER meals
-inhibits gastric emptying
- satiation

2) GLUCAGON-LIKE peptide-1 (GIP-1) on INDEIGESTION
- inhibits gastric emptying
- satiation
which 2 peptides controlling short-term satiation is released from the OXYTINIC cells of the duodenum & jejunum
- in response to what
- effects
1) OXM- AFTER meal
- reduces appetite

2) GHRELIN - BEFORE meals
- increases lipogenesis
- hunger
2 hormones that communicate to hypothalamus to alter energy balance (increase energy burn)
- which cells release them
- which malfunctions in obesity
LEPTIN- adipose

INSULIN- pancreatic ISLET's of Langerhan's (endocrine)
what's the effect of reduced leptin levels (normally produced from adipose cells)
mimics STARVATION = unrestrained appetite, increased fat deposition, reduced energy burn
mimics STARVATION = unrestrained appetite, increased fat deposition, reduced energy burn
how does ORLISTAT work to reduce obesity

SE's
inhibits pancreatic lipase
decreases triglyceride dig & absorption
SHORT-term

x. cramping, severe, diarrhoea
LORCASERIN is a new anti-obesity drug. which receptor does it antagonise
5-HTc receptor antagonists
histology of normal small bowel
JEJUNUM- tallest villi, plicae circularis, goblet cells and crypts of Lieberkuhn

ILEUM- Peyer's patches, smaller villi & crypts, less prominent plicae, goblet cells
JEJUNUM- tallest villi, plicae circularis, goblet cells and crypts of Lieberkuhn

ILEUM- Peyer's patches, smaller villi & crypts, less prominent plicae, goblet cells
2 reasons why the bowel can become ischaemic
OCCLUSION in mesenteric arteries:
- thromboembolism
- atherosclerosis

PERFUSION insufficiency:
- shock
- strangulation
- drugs
- hyperviscosity
which part of the GI wall suffers from ischaemia first (i.e. the most metabolically active)
mucosa- can replace quickly

(muscle damage cannot replace quickly)
3 outcomes of ischaemic bowel
- RESOLUTION
- FIBROSIS, stricture, chronic ischaemia, 'mesenteric angina'
- GANGRENE, perforation, peritonitis, sepsis, death
what's Meckel's diverticulum
what ar ethe complications
incomplete regression of vitello-intestinal duct, outpouching connected to umbilicus 2ft above ileocaecal valve:
X. bleeding, pain, perforation, divertilculitis
incomplete regression of vitello-intestinal duct, outpouching connected to umbilicus 2ft above ileocaecal valve:
X. bleeding, pain, perforation, divertilculitis
primary tumours of small bowel are rare:
- 3 types
LYMPHOMOA- (MALTomo- Bcell derived)

CARCINOID- locally invasve, produce hormones

CARCINOMAS- Chron's & coeliac disease, presents late.
secondary mets to small bowel are common:
from which 3 cancers
ovarian
colorectal
stomach
S&Ss appendicitis
umbilical colic --> constant RIF
vomiting, constipation (or diarrhoea)
tachycardic, shallow breaths, fever
guarding

peritonitis: wash-board rigidity, lay still

↑WCC & CRP
pathology of acute appendicitis
- specific loc of wall?
acute inflammation- neutrophils, eosinophils...
MUCOSAL ulceration 
exudate, pus
acute inflammation- neutrophils, eosinophils...
MUCOSAL ulceration
exudate, pus
3 complications of acute appendicitis
perforation/ rupture --> peritonitis --> sepsis
abscess
fistula
associations with coeliac disease
HLA-B8
dermatitis herpetiformis
childhood DM
pathological features of coeliac disease biopsy
IELs (CD8) damage epithlial cells = villous ATROPHY
MALABSORPTION
↑IELs & ↑inflam cells in lamina propria
PROXIMAL bowel worse
IELs (CD8) damage epithlial cells = villous ATROPHY
MALABSORPTION
↑IELs & ↑inflam cells in lamina propria
PROXIMAL bowel worse
S&Ss coeliac disease
- intestinal
- extra-intestinal
-general
STEATORRHOEA
abdo pain & bloating
N&V
mouth ulcers & angular stomatitis, glossitis (B12 def)
↓weight, fatigue, weak, anaemia, osteomalacia
failure to thrive

asymp!
5 complications of coeliac disease
anaemia
GI T-cell lymphomas (rare)
small bowel carcinoma
gall stones
ulceration & strictures
surgical criteria for bariatric surgery
BMI>35 + co-morbidities
or
BMI>40

achieved 5% weight loss
tried ALL non-surgical Rx
medically & psychologically stable
non-smoker
3 types bariatric surgery
BYPASS - reversible
BAND
SLEEVE
common diseases causing malabsorption 6: CCCCBP
COELIAC
CHRON's
Chronic PANCREATITIS
CIRRHOSIS
Biliary obstruction/ cirrhosis = ↓bile
Post-infection

uncommon: (pancreatic ca, drugs, Short bowel syndrome)
S&Ss malabsorption
diarrhoea, steatorrhoea
↓weight, faitgue
anaemia (pallor, conjunctivae, ulcers, stomatitis, koilonychia)
glossitis
bleeding/ bruising (VitK def)
oedema (↓protein)
Ix's for ?malabsorption
FBC, coagulation (vit K), U&Es (hydration), LFTs (albumin), Ca (vit D def), COELIAC serology (IgA, tTG)

STOOL (fat, infection)
ENDOSCOPY + BIOPSY
RADIOGRAPHY- X-ray, USS, ERCP, CT, MRI
contraindications for artificial enteral feedin gsupport via NG/NG/PEG/PEJ
ulcers
obstruction
perforation
fistulas
facial injury
define acute and chronic intestinal failure
gut not able to supply nutritional & hydrational needs

ACUTE <2wks: mucositis, post-chemo

CHRONIC- short gut syndrome
causes of chronic intestinal failure
SHORT BOWEL SYNDROME- iatrogenic or congenital
Vascular (ischmia)
Neoplasia
Dysmotility
Severe CIRRHOSIS
Iatrogenic
management of short bowel syndrome
supportive/ symptom control -Rx: PPIs, loperamide, codeine

PARENTERAL feeding (long-term)

TRANSPLANT (last resort)
supportive/ symptom control -Rx: PPIs, loperamide, codeine

PARENTERAL feeding (long-term)

TRANSPLANT (last resort)
some complications of parenteral feeding
!!!PNEUMOTHORAX, puncture ARTERY, THROMBOSIS, SEPSIS!!!!
inappropriate use
liver disease
bone disease
line fracture/ break
psychosocial
clinical features of refeeding syndrome
CV & resp FAILURE
bone marrow suppression- immunosuppression
SEIZURES
Metabolic disturbances: ↓K, ↓Mg, oedema, glucose metabolism shift, ↓vits
commonest western cause small intestinal obstruction
adhesion (eg after surgery, prev intraperitoneal inflam)
or
hernia