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Digestive System > Pathology > Flashcards

Pathology Flashcards

1
Q

What is Jaundice?

A

Jaundice is a yellowish discoloration of the skin and mucous membranes caused by hyperbilirubinemia.

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2
Q

At what level of bilirubin does Jaundice becomes visible?

A

Jaundice becomes visible when the bilirubin level is about 2 to 3 mg/dL (34 to 51 micromol/L).

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3
Q

True or False? Conjugated bilirubin can be excreted via the urine (as it is water soluble), whereas unconjugated cannot.

A

TRUE!!!

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3
Q

Under which conditions does albumin binding to unconjugated bilirubin weakens?

A

Acidosis & Certain substances such as salicylates, certain antibiotics .

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3
Q

Fill in the blanks. “ __________ is due to agenetic variantin the UGT1A1 genewhich results in decreased activity of thebilirubin uridine diphosphate glucuronosyltransferaseenzyme.”

A

Gilbert’s syndrome

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4
Q

What are the most common causes of Pre- hepatic Jaundice?

A

Thalassemia

Spherocytosis

Sickle cell anemia

Malaria

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5
Q

What is the treatment for liver cirrhosis?

A

1.Quitting drinking
2. Beta-blockers
3. Intravenous (IV) antibiotics
4. Low-protein diet

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6
Q

What is the treatment for viral hepatitis?

A

1.Antiviral medications
2.Hepatitis vaccination
3. Plenty of rest and fluids

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7
Q

What is the treatment for Primary Biliary Cirrhosis?

A

Bile acids to help with digestion.

Bile-lowering medication.

Antihistamines like diphenhydramine (Benadryl) for itching

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8
Q

What is the treatment for Alcoholic Hepatitis?

A

Quitting alcohol.

Nutrition supplements

Liver transplant, in severe cases

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9
Q

What is the most common cause of Hepatic Jaundice?

A

Gallstones

Pancreatic cancer

Bile Duct cancer

Pancreatitis

Biliary atresia - genetic condition in which you have narrow or missing bile ducts.

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10
Q

Which procedure is used in the treatment of Biliary Atresia?

A

Kasai procedure

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11
Q

What kind of tests should be done during a Jaundice Investigation?

A
  • Liver function tests(LFTs), as summarised in below
  • Coagulation studies(PT can be used as a marker of liver synthesis function)
  • FBC(anaemia, raised MCV, and thrombocytopenia all seen in liver disease) andU&Es
  • Specialist blood tests, as summarised below as part of a liver screen
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12
Q

What type of epithelium lines the Peritoneum?

A

Single sheet of squamous epithelium on thin stroma.

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13
Q

True or False? Peritoneum is sealed in males and open in Females.

A

TRUE!!

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14
Q

What is Peritonitis?

A

Inflammation of the peritoneum and peritoneal cavity (most commonly due to infection).

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15
Q

What are the classification systems of Peritonitis?

A
  • Infective or non-infective (eg. Blood, urine)
  • Localized or generalized
  • Primary or secondary
  • Further sub-classification based on cause
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16
Q

Somatic pain from peritonitis is usually derived from what nerve supply?

A

Nerve supply derived from nerves to overlying wall, T5 to L2
(except diaphragm, C3 to C5)

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17
Q

Visceral pain from Peritonitis is usually derived from what nerve supply?

A

Sympathetic branch of autonomic system (T6-T12 & L1-2)

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18
Q

True or False? Visceral pain is chemical , mechanical and thermal sensitive while somatic is insensitive to chemical , mechanical and thermal conditions.

A

FALSE!! Somatic pain is thermal , mechanical and chemical sensitive while Visceral pain is INSENSITIVE to those.

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19
Q

Fill in the blanks. “ In peritonitis , Visceral pain is ___________, _________ & _________ sensitive.

A

Distention , Traction and Ischaemia

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20
Q

Fill in the blanks. “ Somatic pain is __________ localized while Visceral pain is __________ localized.”

A

Somatic - Sharp & Well localized pain

Visceral - Deep , dull & poorly localized

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21
Q

What are the 3 basic mechanisms of pain?

A

Perforation
Obstruction
Inflammation

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22
Q

What method is used to investigate generally peritonitis?

A

Surgery

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23
Q

What are causes of Primary Peritonitis?

A
  • Bacterial eg. Spontaneous bacterial peritonitis (SBP ) in ascites
  • Chlamydial
  • Fungal
  • Mycobacterial eg. TB in AIDS
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24
Q

True or False? Primary peritonitis is usually polymicrobial while Secondary peritonitis is usually monomicobial.

A

FALSE!! Primary peritonitis is usually monomicobial while Secondary peritonitis is usually polymicrobial.

PM & SP

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25
Q

In which type of Peritonitis is perforation of the GI tract usually a source?

A

Secondary Peritonitis

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26
Q

Which type of peritonitis is normally obscure?

A

Primary Peritonitis

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27
Q

In what type of peritonitis, is the aetiology normally apparent?

A

Secondary peritonitis

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28
Q

What is Tertiary Peritonitis?

A

Persistence or recurrence of intra-abdominal infection following apparently adequate therapy of primary or secondary peritonitis

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29
Q

What are the causes of Tertiary peritonitis?

A
  • Immunocompromised patient
  • Malnutrition
  • Overwhelming infection
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30
Q

What are some specific causes of Peritonitis?

A
  • Appendicitis
  • Perforated Duodenal Ulcer
  • Complicated bowel obstruction
  • Retroperitoneal disease
  • Gynaecological causes
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31
Q

What is the term given to the generalised inflammation of the oral mucosa?

A

Stomatitis

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32
Q

Where is Atresia most commonly located ?

A

Most commonly located at or near the Tracheal birfurcation

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33
Q

What is the incomplete form of Atresia referred to as?

A

Stenosis

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34
Q

What conditions are Oesophageal varisces associated with?

A
  • Portal hypertension
    *.Cirrhosis
  • Budd-Chiari syndrome
  • Hepatic vein thrombosis
  • Portal vein thrombosis
  • Veno-occlusive disease (VOD)
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35
Q

What is Mallory- Weiss syndrome?

A

Partial-thickness esophageal laceration caused by forceful retching (e.g., after alcohol consumption, bulimia, food poisoning), which presents as painful, blood-streaked emesis.

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36
Q

Which condition presents with Hamman’s sign?

A

Boerhaave’s syndrome

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37
Q

What is Hamman’s sign?

A

It is a crunching sound upon Auscultation of the heart due to pneumomediastinum .

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38
Q

True or False? Mallory - Weiss syndrome can be characterized by tansmural tears in the. oesophagus while Boerhaave syndrome can be characterized by longitudinal tears in the oesophagus .

A

FALSE!! MaLLory - Weis syndrome has Longitudinal tears while Boerhaave syndrome has transmural tears.

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39
Q

What is the most common cause of Oesophagitits ?

A

Reflux disease (GERD)

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40
Q

What is Pill- oesophagitis?

A

Pill esophagitis is caused by certain medications becoming lodged in the esophagus (e.g., antibiotics, nonsteroidal antiinflammatory drugs [NSAIDs], bisphosphonates, iron, tetracycline and potassium chloride).

due to pills….. literally

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41
Q

What are the causative agents for patients with infectious oesophagitis?

A

Candidiasis
Herpes Simples Virus - 1
Cytomegalovirus

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42
Q

What is Eosinophilic oesophagitis?

A

Infiltration of oeosinophils in the oesophagus often in atopic patients (food allergies, asthma, dermatitis, etc.)

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43
Q

True or False? Patients with Eosinophillic oesophagitis normally present with similar symptoms for GERD, however antacids have no effect for treament.

A

TRUE!!

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44
Q

What is the treatment for Eosinophillic oesophagitis?

A

Allergen avoidance and Steroids

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45
Q

What are the anatomical and histological features presented with Eosinophillic Oesophagitis?

A

Patient presents with oesophageal rings .

Eospniphils are found more Proximal than distal in the the epithelium.

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46
Q

What are examples of benign Oesophageal tumours?

A

Squamous papilloma
Leiomyoma

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47
Q

What are examples of Malignant Oesophageal tumours?

A

Squamous cell carcinoma
Adenocarcinoma
Neuroendocrine carcinoma
Lymphoma

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48
Q

What is the name of the condition that will give a “ corkscrew” appearance on the Barium swallow of oesophagus?

A

Diffuse esophageal
spasm.

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49
Q

What are oesophageal strictures and what are the most common causes of them?

A

An esophageal stricture is an abnormal tightening or narrowing of the esophagus.

  • It can be due to caustic injury/ingestion , GERD( most common ) and oesophagitis
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50
Q

What is Plummer- Vinson syndrome ?

A

Triad of Dysphagia, Iron deficiencyanemia, Esophageal webs & atrophic glossitis. (“Plumbers DIE”).

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51
Q

What is the name of the condition in which there is Specialized Intestinal metaplasia - replacement of non-keratinized stratified squamous epithelium with intestinal epithelium (non ciliated columnar with goblet cells in distal esophagus?

A

Barrett’s oesophagus

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51
Q

What is the most common cause of Barrett’s Oesophagus?

A

GERD

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51
Q

What is the most common location for Squamous cell oesophageal carcinoma?

A

Middle 1/3 of oesophagus

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52
Q

What is the morphology for Squamous cell oesophageal carcinoma?

A

Polypoid/ Exophytic- 60%
Excavating - 25%
Flat - 15%

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53
Q

Fill in the blanks. “ _____________ & ________ ( disease) can give rise to Squamous cell carcinoma while ___________(disease) give rise to Adenocarcinoma.

A
  • Plummer- Vinson syndrome & Tylosis ( Howel-Evans syndrome) ——-> Squamous cell carcinoma.
  • Barrett’s oesophagus
    ——> Adenocarcinoma
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54
Q

True or False? Constant drinking of substances such as alcohol and fermented milk (mursik) can be associated with developing an Adenocarcincoma.

A

FALSE!! It is associated with Squamous cell carcinoma

55
Q

What is Gastritis?

A

Gastric inflammation and associated mucosal injury found on biopsy.

56
Q

What are the two types of Gastritis ?

A

Acute & Chronic

57
Q

What are the causes of Acute gastritis?

A

NSAID’s / Aspirin
Alcohol
Smoking
ChemoRx drugs
Uraemia
Curling ulcers (Burns)
Cushing’s ulcer - Brain injury
Ischaemia
Sepsis

“Burned by the Curling iron” -curling’s ulcer

“Always CUSHion the brain.”- Cushing ulcer

58
Q

What are the clinical features of Acute gastritis?

A

Asymptomatic
Pain
Nausea/ vomiting
Haematemesis
Melaena ( dark sticky poop)

59
Q

What are the two types of Chronic gastritis?

A

Autoimmune and H.Pylori

60
Q

What are the histological features of Chronic gastritis?

A

Mucosal atrophy
Intestinal metaplasia
No erosion

61
Q

What are the Virulent properties associated with H. Pylori ?

A

U - Urease- which generates ammonia from endogenous urea, thereby elevating local gastric pH around the organisms and protecting the bacteria from the acidic pH of the stomach.

F- Flagella - Increase motility

A- Adhesion - Attachment to foveolar cell surface.

T- Toxins- Cytotoxin-Associated gene A ( SagA) and Vacuolating cytotoxin A ( VacA) genes - involved in ulcer /cancer formation.

“HP makes U FAT!”

62
Q

Fill in the blanks . Complications of H.Pylori gastritis can result in ________, _______, __________ & _______.

A

Peptic Ulcer diseas
Atrophy - intestinal metaplasia & displasia
Adenocarcinoma
MALT lymphoma

63
Q

What is the Pathogenesis of Autoimmune gastritis ?

A

Autoimmune gastritis is associated with immune-mediated loss of parietal cells and subsequent reductions in acid and intrinsic factor secretion.

64
Q

Which type of Chronic gastritis can result in Pernicious , megaloblastic anaemia and iron deficiency anaemia?

A

Autoimmune gastritis

65
Q

Fill in the blanks. “ Autoimmune gastritis is characterized by diffuse damage of the _________ within the body and fundus of the stomach. “

A

Damage of the oxyntic (acid-producing) mucosa within body and fundus of the stomach

66
Q

Where is the most common location for H.Pylori gastritis?

A

Antrum of stomach

67
Q

True or False? H.pylori gastritis has a higher risk of developing Stomach Adenocarcinoma rather than Autoimmune gastritis.

A

FALSE!! Autoimmune has a higher risk of developing an adenocarcinoma

68
Q

True or False? Hypercalcemia can stimulate gastrin production and thereby increase acid secretion.

A

TRUE!!

69
Q

What are the types of peptic ulcer diseases?

A

Gastric Ulcer & Duodenal ulcer

70
Q

Which type of Peptic Ulcer disease is H.Pylori can be the cause in 95% of cases?

A

Duodenal ulcers

71
Q

Fill in the blanks. “ Peptic ulcers are four times more common in the _____________ than in the _______.

A

More common in Proximal duodenum than in the stomach .

72
Q

What are the causes of Peptic Ulcer disease?

A

Helicobacter pylori
Alcohol
NSAIDS
Stress & Smoking
Ischemic process and RL
Bile reflux
Peptic acid secretion
Zollinger-Ellison syndrome
Carcinoid syndrome
Meckel’s diverticulum

73
Q

True or False? Peptic Ulcer diseases gets worse in the night time and/also 1-3 hours after your meal.

A

TRUE!!

74
Q

What is a major histological feature of duodenal ulcers?

A

Hypertrophy of Brunner’s glands

75
Q

What are the types of Gastric polyps?

A

1) Inflammatory & Hyperplastic

2) Fundic GlandPolyps

3) Adenocarcinoma

76
Q

What is the most common Gastric polyp?

A

Inflammatory & Hyperplastic polyps

77
Q

Which type of Gastric polyp involves the APC gene and is treated with PPI therapy?

A

Fundic Gland Polyps

78
Q

What are the common Mestatic sites for Gastric Adenocarcinoma?

A

I - Irish Node (left axillary node)

Killed - Krukenburg tumour ( ovary)

Bianca’s - Blummer Shelf ( Pouch of Douglas)

Sister - Sister Mary Joseph nodule ( periumbilical lymph node)

Vegetable - Virchow’s node ( Supraclavicular lymph node - Trossier’s sign)

79
Q

Where in the stomach is the most common sites for Gastric cancer?

A

Pylorus , Antrum & Lesser curvature

80
Q

What are the different types of Histological classifications of Gastric Adenocarcinoma?

A

Lauren & WHO

81
Q

The Lauren histological classification of Gastric cancer divides it into _______& _______.

A

Diffuse
& Intestinal

82
Q

True or False? The Intestinal type of Gastric Adenocarcinoma is associated with Hy.Pylori.

A

TRUE!!

83
Q

What is the most prominent feature in the Diffuse type of Gastric Adenocarcinoma?

A

Signet-RIng cells

84
Q

True or False? Early gastric cancer invades the Lamina propria.

A

FALSE!! It doesn’t invade it

85
Q

Which type of Gastric cancer has a Linitis plastica (leather bottle stomach) appearance ?

A

Diffuse Gastric Adenocarcinoma

86
Q

Fill in the blanks. “Gastrointestinal Stromal Tumour arsises from _______.”

A

Interstitial cells pf Cajal

87
Q

What are the rules of that follow Meckel’s diverticulum?

A

2% (of the population)
2 feet (proximal to the ileocecal valve)
2 inches (in length)
2 types of common ectopic tissue (gastric and pancreatic)
2 years is the most common age at clinical presentation
2:1 male:female ratio

88
Q

What are the main causes of Bowel Obstruction?

A
  • Hernias
    -Inguinal & femoral canals
  • Surgical sites
  • Bowel adhesions
  • Fibrous bridges
  • Prior surgery, endometriosis
  • Volvulus
  • Intussusception
89
Q

What is Intussusception?

A

Intussusception occurs when a segment of the intestine, constricted by a wave of peristalsis, telescopes into the immediately distal segment.

90
Q

What is the most common cause of intestinal obstruction in children younger than 2?

A

Intussusception

91
Q

What diagnostic tool is also effective in correcting idiopathic intussusception in infants and young children?

A

Contrast enemas

92
Q

What is Hirschsprung’s disease (Congenital agan- glionic megacolon?

A

Hirschsprung disease stems from a congenital defect in colonic innervation. Patients typically present as neonates with failure to pass meconium in the immediate postnatal period fol- lowed by obstructive constipation.

93
Q

Mutations in what genes can cause Hirschsprung’s disease?

A

Tyrosine kinase RET

94
Q

How can one be diagnosed with Hirschsprung’ s disease?

A

Diagnosis is made by demonstrating the absence of ganglion cells in the affected segment.

95
Q

What is the difference between Crohn’s disease and Ulcerative colitis?

A

Ulcerative colitis is limited to the colon and rectum and extends only into the mucosa and submucosa.
- By contrast, Crohn disease, also referred to as regional enteritis (because of frequent ileal involve- ment), may involve any area of the gastrointestinal tract and is frequently transmural.

96
Q

What is the Genetic Determinant present in Crohn’s disease?

A

HLA B-27 & NOD2

97
Q

True or False? Crohn’s disease is more common in Females than in Males.

A

TRUE!!!

98
Q

What are the features of Crohn’s disease?

A
  • Chronic relapsing
  • Granulomatous
  • Uncertain aetiology
99
Q

What are the clinical features associated with Crohn’s disease?

A

Aphthous ulcers , fissures and fistulas,
Creeping fat
Transmural inflammation
Non- casearting granulomas
Lymphadenopathy
Systemic manifestations
Skip lesions
Cobblestone appearance in which diseased tissue
-Crypt abscess
- Paneth cell metaplasia
- Distortion of mucosal architecture

100
Q

What is Dysentery?

A

Painful, bloody diarrhoea, relatively low volume

101
Q

What are the characteristics of Diarrhoeal disorders?

A
  • Secretory
  • High volume isotonic stool
  • Osmotic
  • Unabsorbed luminal solutes ——> hypertonic stool
  • Exudative*
  • Inflammatory, purulent & bloody
  • Deranged Motility
    Malabsorption*
  • Decreased nutrient absorption
102
Q

What are the viruses associated with Infective Enterocolitis?

A
  • Rotavirus - Infants
    Norwalkvirus - Child., Adults
    Adenovirus
103
Q

What are the preformed toxins associated with Bacterial Enterocolitis?

A

S. aureus, Vidrios, C. perfringens

104
Q

What are the Enterotoxins that can cause Bacterial Enterocolitis?

A

E. coli, V. cholerae

105
Q

What are the enteroinvasive bacteria that can cause Bacterial Enterocolitis?

A
  • Salmonella
  • Shigella
  • C. jejuni
  • Yersinia
106
Q

What are the Helminths that can cause Parasitic Enterocolitis?

A

Strongyloides
Ascaris
Hookworm

107
Q

What are the Protozoa that can cause Parasitic Enterocollitis?

A

Giardia
Cryptosporidia

108
Q

What are the symptoms of Malabsorption syndrome?

A
  • Diarrhoea - Bulky, Frothy, Greasy
    (osmotic)
  • Weight Loss
  • Abdominal Distention
  • Borborygmi
109
Q

What is the most common cause of Malabsorption syndrome in Jamaica?

A

Chronic pancreatitis

110
Q

What he most common cause of Malabsorption syndrome in the USA?

A
  • Cystic fibrosis*
  • Celiac disease (Gluten-sensitive enteropathy)
  • Lactose intolerance
  • Chronic pancreatitis
  • Crohn’s disease
111
Q

What are unusual causes of Malabsorption syndrome in USA?

A
  • Tropical Sprue (Post-infectious Sprue)
    Caribbean (not Ja), South and Central America
  • Whipple’s Disease
    Whites 30 - 40 yrs
112
Q

Fill in the blanks. “ The pathogenesis of Crohn’s disease include a combination of genetic susceptibility and abnormalities in: _______, _________ &_________.”

A

*Immune regulation
* Host-microbe interaction
* Epithelial barrier function

113
Q

What are the benign tumours of the Small intestine?

A

Leiomyomas
Adenomas
Lipomas

114
Q

What are the malignant tumours of the small intestine?

A
  • Adenocarcinomas
  • Neuroendocrine tumours*
  • Lymphomas
  • Gastrointesinal stromal tumours*
115
Q

True or False? Neuroendocrine tumours are benign in the ileum, stomach, colon.

A

FALSE!! They are MALIGNANT in the ileum, stomach, colon.

  • They are benign in the rectum and appendix
116
Q

What are the morphological features of an Acute appendicitis?

A
  • Suppurative
  • Gangrenous
117
Q

What are the complications of an Acute appendicitis?

A
  • Abscess
  • Perforation
  • Peritonitis
  • Septicaemia
118
Q

What are the tumours associated with the Appendix?

A
  • Neuroendocrine tumour
  • Mucinous cystic tumours
    adenoma/carcinoma pseudomyxoma peritonei
  • Adenocarcinoma
119
Q

What is Gastrointestinal Bleeding?

A

This is Intraluminal blood loss from anywhere from the mouth to anus

120
Q

What are the classifications of GI bleed?

A

Upper GI bleed
Small bowel (middle GI bleeding)
Lower GI bleeding

121
Q

Where does Small Bowel bleeding take place?

A

Between the ligament of Treitz and Iliocaecal valve

122
Q

Where does Lower GI bleed occur?

A

Distal to the Ileocaecal valve

123
Q

What is an anatomical mark to denote the duodenal junction?

A

The ligament of Treitz

124
Q

What accounts for 75% of all acute GI bleed?

A

Upper Gi bleeding

125
Q

What are the causes of an Upper GI bleed?

A
  • Peptic ulcer - Gastric/duodenal
  • Cancers - oesophageal , gastric, duodenum
  • Erosive oesophagitis
  • Duodenitis
  • Varices
  • Mallory Weis tear
  • Vascular malformation
    *
126
Q

What are the clinical manifestations of an Upper GI bleed?

A
  • Hemetemesis ( vomiting bright red blood)
  • Melena
  • Hematochezia -the passage of fresh blood per anus
  • Nausea
  • Vomiting
  • Retching
  • Epigastric pain
127
Q

Where are lower GI bleeds located?

A

Distal to the ileocecal valve
- bleeding from colon and rectum

128
Q

What are the causes of a Lower GI bleed?

A
  • Diverticular diseases
  • Vascular - Angiodysplasia, Haemorrhoids
    Ischemic collitis
    Post biopsy or post polypectomy bleeding , radiation induced telangiectasia
  • Infectious collitis
    Inflammatory Bowel disease , gastroenteritis
  • Carcinoma
129
Q

What are the clinical manifestations of a Lower GI bleed?

A
  • Hematochezia
    BRBPR( Bright red blood per rectum) or maroon stools.
    *Rarely Melena
  • Associated symptoms- abdominal pain , constitutional symptoms, diarrhoea, constipation , tenesmus (straining), urgency
130
Q

What is used in GI bleeding management?

A
  • Airway protection as needed
  • 2 Large bore IV access(18 G or larger)
  • Volume resuscitation
  • fluid resuscitation with crystalloids
  • Transfusion of blood products if indicated.
  • Correct coagulopathies
  • FFP to normalised deranged PT, PTT
  • Platelets to keep platelets > 50 if actively bleeding
  • Haemoglobin levels
131
Q

What are the blood investigations for GI bleeding management?

A
  • Complete blood count
  • Clotting indices PT,PTT,INR
  • Group and cross match.
  • Urea, creatinine & electrolytes.
132
Q

Upper GI bleed risk stratification is used using what source?

A

Glasgow-Blatchford score (GBS)

133
Q

What is the GBS score for patients with low risk?

A

0-1

134
Q

Lower GI bleed risk stratification is used using what source?

A

Oakland score

135
Q

What is the Oakland score for patients with low risk?

A

Less than 8

136
Q

How is an NG tube useful in GI bleeding management?

A

It is useful for localisation, clear gastric contents prior to endoscopy , detect ongoing bleeding
- discontinued if no active bleeding/drainage.

137
Q

What drugs should be used as treatment in patients with suspected vatical bleeding?

A

Somatostatin analogues - Octreotide or Terlipressin

138
Q

Which diagnostic tool. is most commonly used in detecting a lower GI bleed?

A

Colonoscopy

139
Q

Who are patients with a poor prognosis of a GI bleed?

A

-Over 60 years
- Co-morbidities
- Neoplastoc aetiology
- Hemodynamic instability
- Increasing transfusion requirements.

Digestive System (16 decks)

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