Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Bloc E - Final > Pathology > Flashcards

Pathology Flashcards

1
Q

What us Achalasia?

A

An incomplete LES relaxation, increased LES tone, and esophageal aperistalsis, is a common form of functional esophageal obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the most common cause of esophagitis ?

A

Gastroesophageal reflux disease (GERD): thickening + few eosinophil, responds to proton pump inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Is a GERD has a lot of eosinophils, what can you suspect?

A

Eosino-philic esophagitis: allergic inflammatory disease, presents with dysphagia, food impaction, GERD-like symptoms but affects ALL the oesophagus and responds to corticosteroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is Barrett esophagus?

A

A type of esophagitis which may develop in patients with chronic GERD, is associated with increased risk for development of esophageal adenocarcinoma because there is replacement of the normal squamous mucosa of the lower esophagus with columnar-type epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the most common cause of chronic gastritis ?

A

H. pylori infection: most remaining cases are caused by NSAIDs, alcohol, or autoimmune gastritis. H. pylori gastritis typically affects the antrum and is associated with increased gastric acid production because it attaches to the epithelium of the stomach, H. pylori gastritis induces mucosa-associated lymphoid tissue (MALT) that can give rise to B-cell lymphomas (MALTomas)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is Autoimmune gastritis ?

A

An atrophy of the gastric body oxyntic 
glands, which results in: 1. Decreased gastric acid production 2. Antral G-cell hyperplasia 3. Achlorhydria 4. Vitamin B12 deficiency because anti–parietal cell and anti–intrinsic factor antibodies kills the partietal cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are Peptic ulcers?

A

Ulcers caused by defence mechanisms (mucus, bicarbonate, epithelial regeneration, prostaglandins) or damaging forces (gastric acidity, peptic enzymes, NSAIDs, H pylori, bile reflux)

***DIFFERENTIAL: ulcerated tumour presents as a large ulcer, irregular borders, elevated edges, rough bottom and necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the complications of non-neoplastic stomach diseases?

A
  • lymphoma
  • peptic ulcers
  • cancer
  • intestinal metaplasia
  • gastric atrophy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Common complications of acute pancreatitis?

A
  • Shock
  • Cystic lesions:
  • Pseudocyst formation (MOST COMMON)
  • Mucinous cystic neoplasms: women, body or tail of pancreas, resect
  • Intraductal papillary mucinous neoplasm (IPMNs): male, head of pancreas, resect
  • Serous cystadenoma: anywhere in pancreas, small cysts, benign
  • Panceratic andenoCA
  • Renal/lung failure
  • Ascites
  • Death
  • Chronic pancreatitis

Cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the #1 etiology of chronic pancreatitis?

A

Alcohol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Treatment of pancreatitis?

A

NOTHING BY MOUTH (gotta led pancreas rest)

  • Pain control
  • IV fluids
  • antibiotics if severe
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Autoimmune pancreatitis?

A
  1. IgG4-related: jaundice, mimics cancer, responds to steroid therapy
  2. Non IgG4-related
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Types of neoplasms of pancreas?

A
  • Ductal adenocarcinoma: MOST COMMON, low prognosis
  • Solid pseudopapillary neoplasm: rare, young women, body of tail, resect
  • Pancreatic neuroendocrine (Islet cell) tumour: functional or non-functional
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Cirrhosis – chronic degenerative form?

A
  1. Diffuse liver involvement
  2. Fibrous septation
  3. Nodular regeneration

Can lead to portal hypertension and failure of metabolic functions

Major causes: alcohol, hepatitis C and NASH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Microvesicular steatosis?

A
  • Pregnancy, Reye, drugs
  • Uncommon; fulminant failure, life-threatening
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Steatohepatitis?

A
  • Macrovesicular steatosis, ballooned cells, Mallory bodies
  • Common; EtOH (AST) vs. NAFLD (ALT) (metabolic syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Autoimmune hepatitis?

A
  • Plasma cells
  • ANA, SMA; F>M; give steroids
18
Q

Primary biliary cholangitis?

A
  • Granulomatous florid duct lesion; intrahepatic ducts
  • AMA; F>M; urso, pruritus, osteroporosis
19
Q

Primary sclerosing cholangitis?

A
  • Onion-skin fibrosis, intra- and extrahepatic ducts.
  • M>F; Ulcerative colitis, ERCP, risk of cholangiocarcinoma = BAD, AMA negative
20
Q

Drug toxicity?

A
  • Direct toxicity, hepatic conversion to active toxin or immune-mediated
  • Can look like anything
21
Q

Fulminant hepatic failure?

A
  • # 1 acetaminophen TYLENOL (massive hepatic necrosis)
  • Drugs, HAV, HBV, AIH, BCS, Wilson’s, ischemia, microvesicular steatosis, malignancy, etc
22
Q

Focal nodular hyperplasia?

A

Non-neoplastic, no need to treat

23
Q

Haemangioma

A
  • # 1 primary liver tumour
  • DON’T biopsy = bleeding
24
Q

Hepatocellular adenoma?

A
  • Uncommon, F>M
  • Treatment: discontinue OCP, surgery, surgery
25
Q

Hepatocellular carcinoma?

A
  • Primary malignant tumour of liver
  • Risk factors: cirrhosis, hepatitis C and B, invasion ++, poor prognosis BUT eexception: Fibrolamellar Variant of HCC
26
Q

Liver metastases?

A
  • # 1 liver malignancy
  • Hepatic failure
27
Q

Hereditary hemochromatosis?

A
  • Iron in hepatocytes; C282Y HFE mutation
  • Bronzed diabetics cirrhosis cardiomyopathy; HCC risk; phlebotomy, brown liver
28
Q

Alpha-1 antitrypsin deficiency

A
  • PAS-D droplets in zone 1 hepatocytes
  • PiZZ; emphysema; may present in childhood or adulthood
29
Q

Wilson’s disease?

A
  • Copper in zone 1 hepatocytes
  • Kayser-Fleischer rings (eyes), Parkinson-like, hemolytic anemia, renal injury, vascular diseases
30
Q

Budd Chiari syndrome?

A
  • Hepatic vein thrombosis
  • F>M; polycythemia rubra vera, etc.
31
Q

General features of adenocarcinoma?

A

Malignant epithelial neoplasm with glandular differentiation

32
Q

Precursor lesions of adenocarcinoma?

A
  1. Intestinal metaplasia (change from one type of cell to another)
  2. Adenoma (nuclear enlargement, absent polarity)
  3. Dysplasia
33
Q

General features of squamous cell carcinoma?

A

Malignant epithelial neoplasm with squamous cell differentiation

34
Q

Precursor of squamous cell carcinoma?

A
  1. Squamous cell carcinoma in situ
35
Q

General histologic malignant features?

A
  • necrosis
  • frequent mitosis
  • desmoplastic stroma
  • high nuclear
  • irregular size/shape
36
Q

Oesophagus neoplastic lesions?

A

Adenocarcinoma

Precursor = Barrett in distal oesophagus

Clinical presentation:

  • Symptoms related to GERD
  • Dysphagia
  • Pain (epigastric, retrosternal)
  • Weight loss
  • Anemia: iron deficiency

Squamous cell carcinoma (SCC)

More frequent in >50 YO, more frequent in men

Associated with smoking, alcohol and carcinogens in food, NO Barrett esophagus

Clinical presentation:

  • Small tumors may be asymptomatic
  • Dysphagia, chest pain, weight loss
  • Endoscopy with biopsy is the diagnostic method of choice
37
Q

Types of stomach neoplastic lesions?

A

Adenocarcinoma

  1. Intestinal type: gastric mass with central ulceration
  2. Diffuse (signet ring cell) type: diffuse thickening of the gastric wall and effacement of the gastric folds in the distal stomach, round cells with cytoplasmic mucus accumulation and eccentric nuclei infiltrate
    * Lymph node metastasis

Lymphoma

  1. MALT lymphomas
    • Low-grade B-cell lymphoma
    • Strongly associated with H pylori infection
    • May regress after H pylori eradication
  2. B-cell lymphoma
    • High-grade B-cell lymphoma
    • May arise de novo or in the setting of MALT lymphoma
    • On endoscopy, a large soft mass, sometimes ulcerated, is seen
38
Q

Risk factors of stomach adenocarcinoma?

A
  • H. Pylori infection + low and high grade dysplasia
  • Gastric adenoma
  • Metaplasia
  • Diet rich in smoked salted food and nitrites and poor in fruits and vegetables,
  • Smoking
39
Q

Colorectal neoplastic lesions?

A

Adenocarcinoma

Inherited CRC syndromes:

  1. Familial adenomatous: aggressive, distal colon, hundreds of polyps, colostomy
  2. Hereditary non polyposis colorectal cancer (HNPCC): Lynch syndrome, proximal colon

Precursor adenoma: tubular of villous type, nuclear enlargement, stratification, and lack of maturation

40
Q

Pathways of colorectal adenocarcinoma?

A
  1. Chromosomal instability (85%)
  2. Microsatellite instability (15%), better prognosis
41
Q

Neuroendocrine tumors: carcinoid tumors features?

A

Well-differentiated neoplasm arising in the mucosal neuroendocrine cells in the STOMACH

  1. Type 1: in the background of atrophic gastritis
  2. Type 2: Zollinger-Ellison syndrome
  3. Type 3: sporadic

Clinical presentation:

  • Incidental finding at endoscopy
  • Carcinoid syndrome (flushing, teleangiectasias, cyanosis, bronchoconstriction, edema, hyperperistalsis, pulmonary and tricuspid valvular disease)
42
Q

Gastrointestinal stromal tumors features?

A

Tumors arising from the interstitial cells of Cajal, the pacemaker cells involved in controlling the gastric peristalsis

Bloc E - Final (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions