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1-5 GIT > Anatomical Path > Flashcards

Anatomical Path Flashcards

1
Q

Non-specific symptoms of GIT disease

A
  • Pain
  • Nausea and vomiting
  • Malabsorption – nutrient deficiency
  • Loss of appetite/weight loss
  • Diarrhea
  • Constipation/obstruction
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2
Q

Signs of GIT disease

A
  • Tenderness
  • Abdominal distension
  • Palpable mass
  • Haemorrhage – due to ulceration, can present with anaemia + faecal occult blood
  • Peritonitis due to perforation
  • Systemic infection – sepsis
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3
Q

Vascular pathologies the GIT: arterial and venous

A

Arterial: occlusion results in ischaemia and infarction due to embolism/rupture
Venous: results in congestion, ischaemia with maybe infarction, due to mechanical obstruction

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4
Q

Consequences of infection/inflammation of the GIT

A
  • pain, dysfunction, malabsorption and diarrhoea
  • surface damage = ulceration, haemorrhage, perforation
    Infection - can become septic
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5
Q

Consequences of trauma in the GIT

A
  • Organ damage/rupture – necrosis, dysfunction, peritonitis

* Vascular damage – haemorrhage, haematoma, ischaemia, infarction

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6
Q

AI gastric diseases

  1. atrophic gastritis
  2. coeliac disease
A

Atrophic gastritis - antibodies are produced against the parietal cells of the gastric body. These cells secrete intrinsic factor which is essential for absorption of vitamin B12. Lack of this can result in pernicious (megaloblastic) anaemia.
Coeliac disease - where the gluten in wheat products triggers the body’s immune system to damage the absorptive enterocytes in the small bowel resulting in malabsorption, diarrhoea and anaemia. (not strictly autoimmune)

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7
Q

Signs and symptoms of neoplasm in GIT

A
  • Mass – not often palpable till late
  • Obstruction – dysphagia, constipation
  • Haemorrhage from surface ulceration – anaemia, haematemesis/malena – shock
  • Perforation – peritonitis, tumour seeding
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8
Q

4 layers in mucosa of the GIT

A
  • Squamous epithelium
  • basement membrane
  • lamina propria
  • muscular is mucosae
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9
Q

Layers in the muscularis propria

A
  • inner circular muscular coat
  • outer longitudinal muscle coat
  • Auerbach nerve plexus
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10
Q

What is the GOJ and what cells are there?

A

Gastro-oesophageal junction

Where squamous mucosa of the oesophagus meets the columnar mucosa of the stomach

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11
Q

What is a sliding hernia?

A

Most common hernia, where part of the stomach is pulled up from above the diaphragm
Due to: congenitally short oesophagus or scarring following chronic injury

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12
Q

What is a rolling hernia (AKA paraoesophagheal hernia)

A

Part of the cardiac end of the stomach pushes through the diaphragm rolling up alongside the oesophagus

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13
Q

Causes of GORD

A
  • LES disease
  • hiatus hernia
  • increased volume
  • lifestyle
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14
Q

Clinical issues in GORD

A
  • Mucosal damage
  • infections
  • complications - asthma, aspiration pneumonia, adenocarcinoma
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15
Q

Microscopic findings in GORD

A
  • hyperplastic squamous cell epithelium
  • swollen cells, spongiosis
  • erosions
  • ulcerations
  • inflammatory cells
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16
Q

Eosinophilic oesophagi’s

  1. Cause
  2. Clinical issues
  3. Macroscopic features
A
  1. Allergen
  2. Abdo pain, vomiting, dysphagia, reflux
  3. mucosal rings, webs, stricture, vertical lines or furrows
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17
Q

Risk factors, clinical signs and management of candida oesophagitis

A

Risks: immunosuppression, chemo, steroids, surgery
Clinical: dysphagia
Mx anti fungals

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18
Q

What condition may an Owl’s inclusion be present?

A

Viral oesophagitis - CMV

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19
Q

What is Barrett’s oesophagitis?

A

Metaplasia - change from squamous cells of tubular oesophagus to intestinal type glandular mucosa/mucous secreting cells
Clinical: heartburn, cough, reflux, some no symptoms

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20
Q

2 main types of oesophageal cancer

A
  1. adenocarcinoma - malignant neoplasm with glandular differentiation
  2. squamous cell carcinoma - malignant neoplasm with squamous cell differentiation
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21
Q

Diagnosis of H.Pylori

A

Dyspepsia - urea breath test, serology, stool antigen assay
Endoscopy with biopsy
–Usually biopsy at time of endoscopy and urease breath test

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22
Q

What is AI gastritis and how does it present?

A

Immune response against parietal cells (acid/intrinsic factor)
Clinical - pernicious anaemia, iron deficiency anaemia

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23
Q

What stomach neoplasms can arise from these tissues:

  1. epithelial
  2. mesenchymal
  3. lymphoid
  4. neuroendocrine
A
  1. epithelial - dysplasia, carcinoma
  2. mesenchymal - GI stromal tumour
  3. lymphoid - MALT lymphoma
  4. neuroendocrine - carcinoid (NET)
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24
Q

4 Types of neuroendocrine tumour

A

Type I – secondary to AI gastritis – chronic gastrin hypersecretion
Type II – with Zollinger-Ellison (MEN I)
Type III – solitary, larger
Type IV – rare – parietal cell dysfunction

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25
Q

Most common cause of liver abscess

A

Pyogenic - bacterial in the biliary tract (enteric bacteria)

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26
Q

What is pancreatitis?

A

Inflammatory process caused by blockage of pancreatic bile duct by gallstones or chronic alcohol abuse. Pancreatic enzymes self digest organ and cause necrosis

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27
Q

What is cholangitis?

A

Infection of biliary system due to blockage of common bile duct by gallstone/tumour/stricture

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28
Q

What is cholecystitis?

A

Obstruction of cystic duct by gallstone

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29
Q

What does diverticulitis arise from?

A

Diverticulosis - sac like projections from colonic wall

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30
Q

Pathological findings in diverticulitis

A
  • Local erosion
  • inflammation
  • necrosis of mucosa
  • micro/macro perforation of diverticulum
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31
Q

Classification of peritonitis

A
  1. Primary - monomicrobial
  2. Secondary - polymicrobial usually, leakage of bacteria from bowel
  3. Tertiary - peritonitis in critically ill patient, persisting after mgmt
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32
Q

Empiric antibiotics for Liver abscesses, appendicitis, diverticulitis, acute peritonitis

A

Gentamicin
Amoxicillin
Metronidazole

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33
Q

What is duodenitis?

A

Peptic duodenitis is inflammation and damage to the proximal duodenum secondary to chronic overexposure to gastric acid

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34
Q

H. Pylori duodenal ulcer proposed pathogenesis

A
  • Antral H. Pylori
  • reduced astral D-cell somatostatin
  • XS gastrin release
  • trophic effect on parietal cells
  • increased acid secretion
  • duodenal damage - gastric metaplasia
  • duodenal ulcer
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35
Q

Risk factors for GI events

A
  • age
  • ulcer history
  • high dose NSAID’s
  • major illness
  • smoking/alcohol
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36
Q

Coeliac disease

A

Malabsorption due to chronic immune mediated reaction to gluten

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37
Q

Laboratory test for coeliac disease

A

Tissue transglutaminase - about 90% specific and sensitive

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38
Q

What is Meckel diverticulum?

A

Ileal out-touching due to the persistence of the congenital vitelline duct

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39
Q

Rule of 2’s for Meckel Diverticulum

A

o 2 inches in length (average)

o Located within 2 feet of ileocaecal valve

o Usually symptomatic before age 2

o See in 2% (1-4%) of the population

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40
Q

What can Giardia Lamblia be treated with?

A

Metronidazole

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41
Q

Crohn’s disease

A

¥ Relapsing, discontinuous, transmural granulomatous inflammation from oral cavity to anus

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42
Q

Histological findings in Crohn’s disease

A
  • crypt abscesses
  • granuloma
  • ulceration
  • hypertrophy
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43
Q

Presentation of small bowel adenocarcinoma and risk factors

A

Presentation: abd pain, obstruction, anaemia, GI bleeding, weight loss
Risks: Crohn’s, coeliac’s, polyposis syndromes

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44
Q

What is enterobius vermicularis commonly associated with?

A

Common infection in children, may cause appendix infection

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45
Q

Epithelial and non-epithelial colorectal neoplasms

A 
Epithelial
- adenoma
- adenocarcinoma
Non-epithelial
- NE (carcinoid)
- GI lymphoma 
- GI stromal tumour 
- mesenchymal tumour
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46
Q

What is a polyp?

A

Mass that protrudes into the lumen of the gut

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47
Q

Are adenomas cancer?

A

No - all adenomas are dysplastic, with NO invasion, they become cancer when they start invading

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48
Q

What is dysplasia?

A

Pre-cancerous lesions

  • disordered growth, differentiation and maturation of cells
  • confined to the epithelium
  • show features similar to malignant cells
49
Q

Most common form of colorectal carcinoma

A

Adenocarcinomas (98%) - gland forming

50
Q

Mutations associated with colorectal carcinogenesis

A
  • loss of APC gene
  • defective DNA mismatch repair genes
  • BRAF mutations
51
Q

Risk of colorectal carcinoma is related to number of _____

A

adenomas

52
Q

Peak incidence of colorectal cancer (excl. familial cases)

A

60-70yrs

53
Q

Dietary risks for adenocarcinoma in the colorectal region

A
  • high calorie
  • low fibre
  • refined carbs
  • red meat
  • reduced protective nutrients
54
Q

Most common location of colour-rectal cancer

A
  • rectosigmoid 55%

- caecum/ascending colon 22%

55
Q

Clinical presentation of colorectal cancer

A
  • fatigue
  • anaemia
  • weakness
  • bleeding PR, altered bowel habits
  • screening
  • metastatic disease
56
Q

Colorectal familial syndromes

A
  1. Familial adenomatous polyposis syndrome (FAP)

2. Hereditary non-polyposis colorectal carcinoma (HNPCC)

57
Q

Microvessicular vs macrovessicular steatosis

A

Micro - numerous small lipid droplets present in hepatic cytoplasm (UNCOMMON)
Macro - fat vessicle filling hepatocyte cytoplasm

58
Q

Histological patterns in the liver

A
  1. hepatitis - inflammation
  2. steatosis - fatty
  3. cholestasis - retention of bile
59
Q

Causes of hepatitis

A
  • viral
  • AI
  • drug/alcohol
  • PBC/PSC
60
Q

General histological features of cholestasis

A
  • feathery degeneration of hepatocytes
  • bile plugs
  • cell death w inflamm
  • bile ductule proliferation at edge of portal tracts
  • fibrosis - cirrhosis
61
Q

Intra-hepatic causes of cholestasis

A
  • inborn error
  • drugs (flucloxacillin)
  • primary biliary cirrhosis
  • primary sclerosis cholangitis
62
Q

Pre and post hepatic causes of cholestasis

A

PRE: XS production of bilirubin
POST: obstruction AKA gallstone, tumour etc

63
Q

What is the most common benign and most common malignant tumour of the hepatobiliary system?

A

Benign - haemangioma

Malignant - metastases

64
Q

Histology of malignant hepatocytes

A
  • large nuclei
  • nucleoli
  • mitoses
  • thick liver cell plates
65
Q

Pathogenesis of cholesterol stones

A

• Bile salts and phospholipids render cholesterol soluble in bile
• When bile cholesterol concentration exceeds the solubilising capacity of bile = SUPERSATURATION, cholesterol nucleates into solid cholesterol monohydrate crystals
• Four conditions result in cholesterol GS formation
– Supersaturation
– Hypomotility of GB
– Cholesterol nucleation
– Hypersecretion of mucous traps nucleated crystals leading to aggregation (‘biliary sludge’)

66
Q

Pathogenesis of pigment stones

A
  • Black stones – disorders that lead to elevated levels of unconjugated bilirubin in bile e.g. haemolytic syndromes, severe ileal dysfunction predispose to pigment stone formation (unconjugated bilirubin combines with calcium to form calcium bilirubinate)
  • Brown stones – tend form in bile ducts, contain bacterial degradation products of biliary lipids, calcium salts of fatty acids, unconjugated bilirubin and precipitated cholesterol
67
Q

Acute calculous Cholecystitis

A 
Acute inflammation of GB precipitated in vast majority of cases by GS obstruction of neck or cystic duct
Obstruction - 
– chemical irritation,
– mechanical irritation,
–  ischaemia, – superimposed infection.
68
Q

2 Histological components of the pancreas

A

– endocrine (islets of Langerhan – beta, alpha, delta, PP, D1 and enterochromaffin) and,
– exocrine (80-85%) pancreas – digestive enzymes (acinar cells, ducts: trypsinogen, chymotrypsinogen, proelastase, prophospholipase

69
Q

Pancreas divisum

A

Failure of fusion of the foetal duct systems of dorsal and ventral pancreatic primordia

70
Q

Mechanism of injury of acute pancreatitis

A
  • Pancreatic duct obstruction
  • Primary acinar cell injury
  • Defective intracellular transport of proenzymes within acinar cells
71
Q

Local and systemic complications associated with acute pancreatitis

A

Local complications:
– Peripancreatic fluid collection
– Pseudocyst
– Necrotic collection
– Gastric outlet dysfunction – Splenic and portal vein thrombosis
Systemic complications:
– Exacerbation of pre-existing co-morbidity – Organ failure

72
Q

Autoimmune pancreatitis

A
  • MASS forming inflammatory lesion of the pancreas (may mimic cancer)
  • Two clinicopathological subtypes: – AIP type 1 – IgG4 related disease – AIP type 2 – not IgG4 related
  • Aetiology – multifactorial (genetic factors, bacterial infection, autoimmunity)
  • Treatment is with steroids
73
Q

Define cirrhosis

A

Diffuse alteration of the normal architecture by fibrous septa separating nodules of regenerating hepatocytes.

74
Q

Micronodular vs macro nodular cirrhosis

A

Micro <3mm

75
Q

Clinical signs and symptoms of cirrhosis

A
  • No symptoms, abnormal LFTs
  • Non-specific symptoms and signs Malaise
  • Abdominal pain and tenderness in RUQ
  • Hepatomegaly - smooth or irregular (cirrhosis)
  • Signs/symptoms of liver failure
  • Multi-organ failure / death
76
Q

Liver functions

A
  • mechanical filter
  • detoxification
  • part of digestive system
  • protein manufacturing
77
Q

Cirrhosis effect on mechanical filtering of liver

A
  • portal HTN due to increasing obstruction of blood flow through liver
  • abdominal swelling
  • haematemesis and malena
  • ascites and jaundice
78
Q

Cirrhosis effect on detoxification

A
  • nitrogens, encephalopathy, mental confusion
  • bile, jaundice, itch
  • oestrogen decreased breakdown, gynaecomastia, hypogonadism, spider nave, palmar erythema
79
Q

Cirrhosis effect on digestion

A
  • decreased bile excretion, diarrhoea, steatorrhoea

- decreased metabolism,, LOA and LOW, wasting

80
Q

Cirrhosis effect on protein manufacture

A
  • decreased albumin production - abdominal and leg swelling, ascites and peripheral edema
  • decreased clotting factor production (2, 7, 9, 10) - bruising and coagulopathy
81
Q

Causes of cirrhosis

A
  • alcohol/drug
  • viral hepatitis
  • AI hepatitis
  • metabolic diseases
  • biliary tract disease
  • idiopathic
82
Q

Acute liver failure

A

Acute liver failure is loss of liver function that occurs rapidly — in days or weeks —usually in a person who has no pre-existing liver disease.

hyperacute is within 1 week, acute as 1-4 weeks and subacute as 4–12 weeks

Aka fulminant hepatic failure.

The complications are;
hepatic encephalopathy
impaired protein synthesis (as measured by the levels of serum albumin and the prothrombin time in the blood).

83
Q

Indications for liver transplantation

A
  • end stage chronic liver disease
  • acute liver failure
  • hepatic neoplasms
84
Q

Issues in liver transplantation

A
  • native diseased liver
  • donor liver disease
  • preservation injury
  • rejection
  • complications
  • recurrent disease
85
Q

Donor liver disease

A
  • macro vesicular steatosis
  • haemosiderosis
  • chronic hepatitis
  • primary or secondary tumour
86
Q

Preservation injury

A

Period of ischaemic time followed by reperfusion

Manifests in the first two weeks as functional cholestasis, poor function or non-function

87
Q

Histological triad for the diagnosis of acute liver rejection

A
  1. PT inflammation
  2. BD damage
  3. portal vein/central vein endothelialitis

Banff scheme - grading into mild, mod or severe acute rejection

88
Q

Acute vs chronic liver rejection

A

Acute - “An immunological reaction to the presence of a foreign tissue or organ which has the potential to result in graft dysfunction and failure”

Chronic -
“An immunologic injury to the allograft, which usually evolves from severe or persistent acute rejection and results in potentially irreversible damage to the bile ducts, arteries and veins”

89
Q

Complications of liver transplant

A

Biliary anastomosis

Vascular anastomoses

Immunosuppression

  • Infection
  • Post transplant lymphoproliferative disorder - Other malignancies
  • Drug toxicity
90
Q

Immunosuppression complications in liver transplants

A

Infection risk increased
Can occur anytime after transplant
significant cause of mortality and morbidity

Fungal - aspergillus, candida, crytptococcus
Viral - CMV, EBV
Bacterial

Malignancy

Drug toxicity

91
Q

Congenital anomalies of the kidney (4)

A
  1. Agenesis of the kidney
  2. Hypoplasia
  3. Ectopic kidneys
  4. Horseshoes kidneys
92
Q

What is agenesis (Potter’s syndrome) of the kidney? and what are the subtypes?

A

Complete absence of one or both kidneys due to major disruption of the matenephric development at an early stage

  1. Bilateral genesis (Potter’s syndrome) - incompatible with life
  2. Unilateral genesis - usually asymptomatic
93
Q

What can be seen on Potter’s facies?

A

Due to severe oligohydramnios and secondary to bilateral renal agenesis

  • large low set ears
  • wide set eyes
  • flattening of nose
  • receding chin
  • prominent skin folds below eyes
94
Q

Where are ectopic kidneys usually located? and why is it there?

A

Usually just above the pelvic brim or within the pelvis - due to failure of kidney to ascend

95
Q

What are horseshoe kidneys?

A

Fusion of the upper or lower poles of the 2 kidneys but each kidney still has its own pelvis and ureter

96
Q

Clues to malignancy in simple renal cysts

A
  • Multiple septa
  • Thickened wall of cyst
  • Solid areas within of around the cyst
97
Q

What is cystic renal dysplasia

A

• Malformation of the kidney
• Unilateral or bilateral
• Often associated with obstruction/reflux
• Consists of varying sizes
¥ Common cause of an abdominal mass in infants

98
Q

What is polycystic kidney disease characterised by and what are the two types?

A

Numerous fluid filled cysts in the kidneys, causing massive enlargement

  1. Autosomal dominant PKD
  2. Autosomal Recessive PKD
99
Q

Prevalence of Autosomal dominant and recessive PKD

A

Dom: 1/500
Rec: 1/20,000

100
Q

Features of ADKPD

A

¥ Cyst formation begins in-utero
¥ Cysts grow over time, compress surrounding renal tissue, cause renal falure
¥ Kidneys become massive – up to 4kg
¥ Patients present in their 30s-50s with flank pain due to abdominal mass or renal stones, pain from hemorrhage into a cyst, haematuria, hypertension

101
Q

When does autosomal recessive PKD present?

A

infancy/childhood

102
Q

What is hydronephrosis?

A

Water inside the kidney

  • distension and dilatation of the renal pelvis and calyces caused by obstruction of free flow of urine from the kidney
  • leads to atrophy of the kidney
103
Q

Types of kidney stones

A
  1. Calcium oxalate
  2. Uric acid
  3. Struvite – magnesium ammonium phosphate
  4. Calcium phosphate
  5. Cysteine
  6. Others – xanthine, drug related
104
Q

Risk factors for calcium containing stones

A 
¥	Dehydration 
¥	Hypercalciuria 
¥	Hyperoxaluric
¥	Hyperuricosuric
¥	Low urine volume
105
Q

Uric acid stones risk factors

A 
¥	Dehydration 
¥	Acidic urine 
¥	Hyperuricaemia (gout)
¥	Chronic diarrhea 
¥	Diabetes
106
Q

Complications of urolithiasis

A

¥ Silent
¥ Pass into the ureters pain and obstruction
¥ Ulceration and bleeding haematuria
¥ Infection

107
Q

Pyelonephritis

A

Inflammation of the kidneys, calyces and renal pelvis (acute or chronic)

108
Q

Causes and complications of acute pyelonephritis

A

Bacterial infection from lower urinary tract or bloodstream

Complications:

  • papillary necrosis
  • pyonephrosis
  • perinephric abscess
  • urosepsis
109
Q

Two types of chronic pyelonephritis

A
  1. reflux nephropathy

2. Chronic obstructive pyelonephritis

110
Q

What is Xanthogranulomatous pyelonephritis?

A

Type of chronic pyelonephritis
¥ Accumulated of foamy macrophages – yellow
¥ Associated with obstruction, protues infection

111
Q

What is analgesic nephropathy?

A

¥ Chronic renal disease caused by XS intake of analgesis mixtures
¥ Characterized by chronic tubulointerstitial nephritis and papillary necrosis

112
Q

Conditions that can result in papillary necrosis

A

¥ Analgesic nephropathy
¥ Diabetes
¥ Infection
¥ Obstruction

113
Q

____% of people with diverticulosis develop diverticulitis

A

15%

114
Q

How does interferon treatment work in hepatitis B/C infections?

A

Blocks viral mRNA synthesis and protein synthesis making non-infected cells resistant to infection

115
Q

What indicates HBV immunity?

A

HBaAB level >10IU/ml

116
Q

Which hepatic enzymes are elevated in hep A, B and C?

A

ALT + AST

117
Q

Pathogenesis of UC and Crohn’s

A

Crohn’s - TH1 and TH17 mediated process

UC - atypical TH2 disorder

118
Q

What mutations are present in all coeliacs?

A

HLA DQ2 + HLA DQ8

119
Q

What is the relevance of Anti-tTG in coeliac disease?

A

Tissue transglutaminase (tTG) is an enzyme involved in gluten metabolism. If present, tTG-Abs are highly indicative of coeliac disease in those with suggestive symptoms and referral for endoscopy is required to confirm diagnosis. However tTG-Abs are only present after significant gluten consumption over a significant period

1-5 GIT (7 decks)

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