Gupta - Pathology Flashcards
1
Q
What do you see here? Types?
A
- Stress-related mucosal disease: punctate erosions
- Most critically ill pts admitted to hospital ICU’s have histo evidence of gastric mucosal damage -> cause likely ischemic
1. Most common in ppl with shock, sepsis, or severe trauma - CURLING: in proximal duodenum, and assoc with severe burns or trauma
- CUSHING: gastric, duodenal, and esophageal ulcers in ppl w/intracranial disease -> high incidence of perforation
2
Q
What is this? Epi? Symptoms?
A
-
Esophageal mucosal web: idiopathic, ledge-like protrusions of mucosa that may cause obstruction
1. Fibrovascular CT + overlying epithelium - EPI: women, age 40, GERD, chronic graft-versus-host disease, or blistering skin diseases
- In upper esophagus, may be accompanied by iron-deficiency anemia, glossitis, & cheilitis as part of the Paterson-Brown-Kelly or Plummer-Vinson syndrome
- Main symptom non-progressive dysphagia assoc with incompletely chewed food
3
Q
What do you see in these appendiceal histo images?
A
-
Mucinous neoplasms: invasion through appendix wall can lead to intraperitoneal seeding and spread (may be mistaken for ovarian tumors in women)
1. Advanced cases fill abdomen with tenacious, semisolid mucin -> pseudomyxoma peritonei - May be held in check for yrs by repeated debulking but, in most instances, follows inexorably fatal course
- Do NOT break these open in surgery
- NOTE: mucocele (dilated appendix filled w/mucin) may be obstructed appendix w/inspissated mucin or be mucinous cystadenoma /cystadenocarcinoma
1. Can also get mucoceles on lip
4
Q
Etiology and molecular markers of SCC in the oropharynx?
A
- 95% of cancers of head/neck SCC
- 70% of SCC in oropharynx (NOT the oral cavity), esp those involving tonsils, base of tongue, and pharynx, harbor oncogenic variants of HPV, esp HPV-16
1. Better long-term survival if HPV+ cancer: over-express p16, cyclin-dependent kinase INH - Typically advanced stage at dx; not amenable to screening, and may have multiple primary sites
- Genetic alterations w/molecular signature consistent w/tobacco carcinogen-induced cancers
5
Q
What are the features of Menetrier disease?
A
- Rare, acquired pre-malignant disease of stomach: associated with adenocarcinoma
- Mutations of TGF-alpha, leading to massive gastric folds and excess mucous production -> gastropathy
- 30-60 y/o’s
- Limited inflammation in body and fundus of stomach
- SYMPTOMS: hypoproteinemia, weight loss, diarrhea
6
Q
What are these? Difference?
A
- OMPHALOCELE (left): closure of abdominal muscles incomplete and abdominal viscera do not return to abdomen from umbilical cord, remaining in a ventral amnioperitoneal membranous sac
1. May be repaired surgically, but as many as 40% of these infants have other birth defects - GASTROSCHISIS (right): similar to omphalocele, but it involves all of the layers of the abdominal wall, from the peritoneum to the skin; herniation through muscle near belly button (less frequently assoc with other defects than omphalocele)
7
Q
What is going on here?
A
- Sialadenitis: inflammation of salivary glands
- Can be infectious (viral, bacterial) or noninfectious (Sjogren syndrome, sarcoidosis, radiation)
- Staphylococcus aureus is often the pathogen (see attached image)
- Acute sialadenitis typically involves parotid gland, which becomes swollen, erythematous, and painful + purulent discharge drains from the duct
8
Q
What are the features of fundal gland polyps?
A
- Age 50
- Parietal and chief cells
- No inflammation or symptoms
- Risk factors: PPIs, familial adenomatous polyposis (FAP)
- Association with gastric adenocarcinoma only in syndromic FAP
9
Q
What happened here?
A
- Graft-vs-host disease: after hematopoietic stem cell transplant -> small bowel and colon involved in most cases
- 2o to donor T-cells targeting Ag’s on recipient’s GI epithelial cells, but lamina propria lympho infiltrate is typically sparse
- Epithelial apoptosis, particularly of crypt cells, is the most common histologic finding
- Apoptotic debris in this image
10
Q
What do you see here? Epi?
A
- Erythroplakia: much less common than leukoplakia
- Much more ominous than leukoplakia: virtually all (about 90%) disclose severe dysplasia, carcinoma in situ, or minimally invasive carcinoma
-
Epi: associated with tobacco use
1. People 40-70 y/o
2. Typically males
3. Can occur anywhere in oral mucosa
11
Q
What is this? Epi? Radiology? Histo? Tx?
A
- Odontogenic keratocyst (OKC; aka, keratocystic odontogenic tumor): assoc w/basal cell nevus syn
- EPI: posterior mandible in 10-40-y/o males
- RADIOGRAPH: well-defined unilocular or multi-locular radiolucencies
- HISTO: cyst lining a thin layer of keratinized stratified squamous epithelium w/prominent basal cell layer and corrugated epithelial surface (key to diagnosis)
- TX: requires complete removal of lesion b/c locally aggressive, and recurrence rates for inadequately removed lesions can reach 60%.
12
Q
What are these?
A
- Mallory-Weiss tears -> lacerations: longitudinal mucosal tears near gastroesophageal junction
- Most often associated with severe retching or vomiting secondary to acute alcohol intoxication
- Do not generally require surgical intervention, and healing tends to be rapid and complete
13
Q
What is going on here?
A
- Gastric antral vascular ectasia (GAVE): watermelon stomach -> red and white alternating mucosa (ex: can be seen in systemic sclerosis or cirrhosis)
- Can be recognized endoscopically as longitudinal stripes of edematous erythematous mucosa that alternate with less severely injured, paler mucosa
1. Erythematous stripes are ectatic (dilated) mucosal vessels - HISTO: antral mucosa shows reactive gastropathy with dilated capillaries containing fibrin thrombi
- Patients may present with occult fecal blood or iron deficiency anemia
14
Q
What do you see here?
A
- Mucoepidermoid carcinoma: variable mixtures of squamous, mucus-secreting, and intermediate cells
- 15% of all salivary gland tumors; 60-70% in parotid
-
Grade is important determinant of 5-year survival:
1. Low-grade = 90% (indolent)
2. High-grade = 50% - Most comm malignant salivary gland tumor in kids
- Mucin stain (pink) can be helpful for diagnosis
15
Q
What is this?
A
- Esophageal ring, or Schatzki ring: similar to webs, but circumferential and thicker
- Include mucosa, submucosa, and, occasionally, hypertrophic muscularis propria
16
Q
What are the features of gastric adenomas?
A
- Age 50-60
- More common in the antrum than the body
- Dysplastic, intestinal cells
- Variable amt/types of inflammation
- Similar symptoms to chronic gastritis
- Risk factors: chronic gastritis, atrophy, intestinal metaplasia
- Frequent association with gastric adenocarcinoma
17
Q
What are the 2 main types of appendiceal tumors?
A
- Carcinoid
- Mucinous neoplasms
18
Q
What is the most common manifestation of esophageal malformations?
A
- Proximal esophageal atresia (B)
- Esophagus continuous with the mouth ending in a blind loop superior to the sternal angle
- Distal esophagus arises from the lower trachea or carina
19
Q
What is this? Describe the histo. Epi?
A
- Leukoplakia: white patch or plaque that can’t be scraped off, and can’t be characterized clinically or pathologically as any other disease
- Premalignant until proven otherwise; much lower threshold for calling things in oral cavity dysplasia vs. the cervix
- HISTO -> severe dysplasia characterized by:
1. Nuclear and cellular pleomorphism
2. Numerous mitotic figures, and
3. Loss of normal maturation - EPI: associated with tobacco use, 40-70-y/o males; can occur anywhere in oral mucosa
20
Q
What are these (appendiceal)?
A
- Mucinous neoplasms: start worrying when cells become elongated and hyperchromatic
- TOP: tumor cells with abundant cytoplasmic mucin, enlarged, hyperchromatic basal nuclei, and minimal cytologic atypia
- BOTTOM: epi cells that are cytologically low grade, similar to neoplastic cells in the appendix
- ATTACHED: peritoneal mucin deposits with scant strips and clusters of mucin-containing epithelial cells (pseudomyxoma peritonei)
21
Q
What is this? Histo?
A
- Carcinoid tumor: most common tumor of appendix
- Usually incidental, and almost always BENIGN
- Frequently forms solid, bulbous swelling at distal tip of the appendix (like in the image on front of card)
1. Golden, yellow appearance - Although intramural and transmural extension may be evident, nodal metastases are very infrequent, and distant spread is exceptionally rare
- HISTO: nested, bland cells with salt and pepper chromatin, like all NE tumors (see attached)
22
Q
What is the most common form of congenital intestinal atresia?
A
- Imperforate anus: due to failure of cloacal diaphragm to involute
- These infants fail to pass meconium
23
Q
What is this (anorectal biopsy)? Most significant prognostic factors?
A
- Squamous cell carcinoma: assoc w/HPV-16 (most common anorectal malignancy)
-
Tumor size (T stage) & nodal status (N stage) are most significant prognostic factors for pts with anal squamous cell carcinoma (SCC)
1. 5-year survival by stage:
T1 and T2 – 86%
T3 – 60%
T4 – 45%
N0 – 76%
Node-positive – 54%
24
Q
What are the features of Zollinger-Ellison syndrome?
A
- Gastrinoma, leading to peptic ulcers and neutro inflammation
- INC HCl released by parietal cells in the fundus of the stomach
- No association with adenocarcinoma
- Risk factor: MEN-1
- Around age 50
25
Q
What is this? Describe 3 types.
A
- Esophageal diverticulum: outpouching of mucosa through muscular layer of the esophagus
- Can be asymptomatic or cause dysphagia and regurgitation
- Dx by barium swallow; sx repair rarely required
- Several types, each of different origin:
1. Zenker (pharyngeal): posterior outpouchings of mucosa/submucosa through cricopharyngeal muscle; lack of coordination b/t pharyngeal propulsion and cricopharyngeal relaxation
2. Midesophageal (traction): traction from mediastinal inflam lesions or motility disorders
3. Epiphrenic: just above diaphragm and usually accompanies motility disorder (achalasia, diffuse esophageal spasm)
26
Q
What do you see here?
A
- Thyroglossal duct cyst: thyroid anlage begins in foramen cecum at base of tongue, and descends to midline location in anterior neck in devo
- Remnants can persist, and are lined by stratified squamous epi when located near base of tongue, or pseudostratified columnar epi in lower locations -> variable histo appearance makes anatomic location important for diagnosis
- CT wall of cyst may harbor lymphoid aggregates or remnants of recognizable thyroid tissue -> tx is EXCISION
27
Q
What do you see in these images?
A
- Viral esophagitis
- GROSS: postmortem specimen with multiple, overlapping herpetic ulcers in the distal esophagus
- TOP RIGHT: multinucleate squamous cells containing herpesvirus nuclear inclusions
- BOTTOM RIGHT: CMV-infected endothelial cells with nuclear and cytoplasmic inclusions -> can be a real problem in people with UC and Crohn’s
28
Q
What are these? What are the divisions of the anal canal? Carcinomas?
A
- Condyloma acuminatum: can be precursor lesions to pure squamous cell carcinoma of the anal canal (freq associated w/HPV infection)
- DIVISIONS (1/3rds):
1. Upper zone: columnar rectal epi
2. Middle: transitional epithelium
3. Lower: stratified squamous epi -> below dentate/pectinate line (palpable on exam) - NOTE: carcinomas of anal canal may have typical glandular or squamous patterns of differentiation
1. Tend to be squamous below dentate line, but more mucosal, and adeno above (only 5%)
29
Q
What is this?
A
- Diaphragmatic hernia: incomplete formation of the diaphragm allows abdominal viscera to herniate into the thoracic cavity
- When severe, space-filling effect of the displaced viscera can cause pulmonary hypoplasia that is incompatible with life
- Liver in thoracic cavity in image on the front of card, and bowel in left side of the thoracic cavity in the attached imaging
30
Q
What is this?
A
- Branchial (cervical lymphoepithelial) cyst: vast majority thought to arise from remnants of 2nd branchial arch -> young adults (20-40-y/o)
- Upper, lateral aspect of the neck along the sternocleidomastoid (SCM) muscle
- MICRO: fibrous walls, usually lined by stratified squamous or pseudostratified columnar epithelium
1. Cyst wall typically contains lymphoid tissue with prominent germinal centers
31
Q
What is going on here?
A
- Esophageal graft-vs-host disease
- HISTO features similar to those in skin, and include:
1. Basal epithelial cell apoptosis,
2. Mucosal atrophy, and
3. Submucosal fibrosis without significant acute inflam infiltrates (ex: in skin biopsy, can have just 1-2 lymphos and some dyskeratotic cells) - Going to see these effects in squamous mucosa b/c turning over rapidly -> GI tract a key region
32
Q
What is this?
A
- Hairy leukoplakia: hyperkeratosis + acanthosis (diffuse epidermal hyperplasia)
- “Balloon” (glycogenated) cells in the upper spinous layer
- Elongation of the epidermis
33
Q
What is the most frequent site of ectopic gastric mucosa in the GI tract? Consequences? Other sites?
A
-
Upper 1/3rd of esophagus -> inlet patch: generally asymptomatic, but gastric mucosal acid can cause dyphagia, esophagitis, Barrett’s, or adenocarcinoma (rarely)
1. Can also mimic invasive cancer b/c may be present in any layer of the wall - Gastric heterotopia (small patches of ectopic gastric mucosa in small bowel, colon) may present w/occult blood loss b/c peptic ulceration of adjacent mucosa
- NOTE: ectopic pancreatic tissue less common, but can be found in esophagus or stomach
34
Q
Describe the progression of normal oral mucosa to SCC (image: gross, histo, molecular).
A
- Note that the SCC in the last set of images is invasive
- Molecular: p16 -> p53 -> Cyclin D
35
Q
What do you see here? Associated pathology?
A
- Sialolith (stone) -> can cause chronic sialadenitis if recurrent or persistent ductal obstruction
- Episodic pain and swelling, usually at mealtime
- Submandibular involvement may include persistent enlargement
-
Tx: sialolith removal, if appropriate
1. Sx removal of the gland may be indicated for chronic sialadenitis
36
Q
This histo is from the anal canal - what is it?
A
-
Squamous cell carcinoma: most common anorectal malignancy -> HPV-16
1. Atypical cells infiltrating into the mucosa - NOTE: adenocarcinoma only 5% of anorectal malignancies, and associated with HPV-18
37
Q
What is going on here?
A
- Cholesteatoma: assoc w/chronic otitis media
- Non-neoplastic, cystic lesions 1-4 cm in diameter, lined by keratinizing stratified squamous epithelium or metaplastic mucus-secreting epithelium, and filled with amorphous debris
- Can erode locally and cause destruction in middle and internal ear
- Like an epidermal inclusion cyst in the ear
38
Q
What happened here?
A
- Boerhaave syndrome: less common, but more serious than Mallory-Weiss tears; characterized by transmural tearing and rupture of distal esophagus
- Catastrophic event produces severe mediastinitis and generally requires SX INTERVENTION
- B/c pts can present w/severe chest pain, tachypnea, and shock, initial differential diagnosis can include myocardial infarction
- Contrast extravasation from distal esophagus in the image on front of the card
39
Q
What do you see here?
A
- Hairy leukoplakia: not uncommonly the first sign of systemic disease (as oral lesions often are)
- Distinctive oral lesion on lateral border of tongue
- Associated with immunocompromised patients
- Caused by EBV
- Unlike thrush (candida), it can’t be scraped off
40
Q
8 y/o presents with right lower quadrant tenderness and nausea, the white count is elevated as is the serum CRP. An appendectomy is performed. What is the diagnosis?
A
- Acute appendicitis with Enterobius vermicularis (pinworm)
- NOTE: kids, in general, have more germinal centers and lymphos in their GI tract
41
Q
What are the features of hyperplastic gastric polyps?
A
- Age 50-60
- Mucous cells
- Neutro and lympho inflammation
- Similar symptoms to chronic gastritis
- Risk factor: H pylori
- Occasional association w/gastric adenocarcinoma
42
Q
What is congenital hypertrophic pyloric stenosis? Presentation?
A
- Muscle hypertrophy, so outlet obstruction from the stomach -> can go in and correct this surgically
- 3-5x more comm in males; 1 in 300-900 live births
- Generally presents b/t 3rd and 6th wks of life as new-onset regurgitation, projectile, non-bilious vomiting after feeding, freq demands for re-feeding
- Physical exam reveals firm, ovoid, 1-2cm abdominal mass
43
Q
What are 4 causes small bowel obstruction? Most common? Clinical manifestations?
A
- Clinical manifestations: abdominal pain, distention, vomiting, and constipation
- HERNIAS: most frequent cause worldwide
- INTUSSUSCEPTION: most comm cause in kids <2; infant cries from abdominal pain, then is fine, then relapses (can also have bloody stool and sausage feeling on palpation in PE)
- VOLVULUS: intestine doesn’t adhere to abdominal wall correctly, and can get twisted around itself (more common in children)
- ADHESIONS: post-surgery
44
Q
What is this? Gross appearance?
A
- Carcinoid tumor: most common tumor of appendix
- Nested, bland cells with salt and pepper chromatin, like all NE tumors
- Usually incidental, and almost always BENIGN
- GROSS: frequently forms solid, bulbous swelling at distal tip of the appendix (see attached)
1. Golden, yellow appearance - Although intramural and transmural extension may be evident, nodal metastases are very infrequent, and distant spread is exceptionally rare
45
Q
What is this? Histo? Tx?
A
- Dentigerous cyst: originates around crown of an unerupted tooth
- RADIOGRAPH: unilocular lesions (1 chamber) most often assoc w/impacted 3rd molar (wisdom) teeth
- HISTO: lined by thin layer of stratified squamous epithelium w/dense chronic inflam cell infiltrate
- TX: complete removal of the lesion is curative
- Association with ameloblastoma -> locally invasive tumors in mandible, radiolucent “soap bubble”
46
Q
What is this? Who gets it?
A
- Pleomorphic adenoma: middle-age F w/painless, slow-growing, movable, non-tender, firm mass
- Typically round, well-circumscribed, and may have a rubbery texture
- Benign mixture of ductal (epi) and myoepithelial cells -> both epi AND mesenchymal differentiation
- NOTE: carcinomas can arise in these -> sudden rapid growth (aka, carcinoma ex pleomorphic adenoma)
47
Q
What do you see here? Describe the characteristic histo.
A
- Pleomorphic adenoma: benign mixture of ductal (epi) and myoepi cells -> both epi and mesenchymal differentiation
- Epithelial elements dispersed throughout matrix, and varying degrees of myxoid, hyaline, chondroid (cartilaginous), and even osseous tissue
- Epithelial component + background mucin-like supporting material common
- May advance to carcinoma, in some cases
48
Q
What are the 3 most common tumors in the salivary glands?
A
- Pleomorphic adenoma (50%): mixed tumor
- Mucoepidermoid carcinoma (15%)
- Warthin tumor (5-10%)
49
Q
What is going on here? Causes? Dx? Presentation?
A
- Acute appendicitis: appendix is a normal true diverticulum of cecum prone to acute/chronic inflam
- Initiated by progressive INC in intraluminal pressure that compromise venous outflow
1. 50-80% of cases associated with overt luminal obstruction, usually by a FECALITH: small stone-like mass of stool - DX: requires neutro infiltration of muscularis propria (inflam throughout the wall)
1. Mucosa shows ulceration and undermining by an extensive neutrophilic exudate here - PRESENTATION: epigastric pain that slowly moves to right lower quadrant
50
Q
What is this?
A
- Fungal esophagitis: almost always Candida
- Parakeratosis of the esophagus
- Acute inflammation: may be less in young, or immunosuppressed people
- Pseudohyphae diving down in the attached image
51
Q
What is this?
A
- Mucinous neoplasm in the appendix
- Typically display a circumferential growth pattern in appendiceal mucosa w/variable papillary architecture
- Glands much more elongated, and more cytoplasm: spitting out mucin
- This example is probably benign
52
Q
What is the most common true diverticulum?
A
- Meckel diverticulum (ileum): failed involution of the vitelline duct (involves all 3 layers)
-
Law of 2’s: 2% of the population
1. Within 2 feet (60 cm) of the ileocecal valve
2. About 2 inches (5 cm) long
3. Twice as common in males
4. Most often symptomatic by age 2 (only about 4% are ever symptomatic) - Can have ectopic tissue in these, which can make them symptomatic
53
Q
What is this? Who gets it?
A
- Warthin tumor: middle-age M smokers; painless
- Benign, but can be bilateral; almost exclusively in the parotids
- Epithelial + lymphoid elements -> follicular germinal center beneath the epithelium
- Cystic spaces separate lobules of neoplastic epi consisting of double layer of eosinophilic epithelial cells based in a reactive lymphoid stroma
- Often do FNA and describe what they pull out as “motor oil” -> dark, thick fluid (cystic)
54
Q
What nodules and tumors can be found in the liver?
A
- Nodular hyperplasia(s)
- Benign neoplasms
1. Hepatocellular adenomas
2. Hemangiomas - Malignant Tumors:
1. Hepatoblastoma
2. Hepatocellular Carcinoma (HCC)
3. Cholangiocarcinoma (CCA)
4. Other Primary Hepatic Malignant Tumors
5. Metastasis: colon, lung, and breast
55
Q
What is this?
A
- Focal nodular hyperplasia: well-demarcated, but poorly encapsulated nodule, up to many cm in diameter -> “central scar” is the buzz word
- Spontaneous mass lesion in an otherwise normal liver, most often in YOUNG to middle-aged adults
- Central gray-white, depressed stellate scar from which fibrous septa radiate to the periphery
- Not much clinical significance
56
Q
What are the 2 types of nodular hyperplasia? Common factor?
A
- TYPES: 1) focal nodular hyperplasia and 2) nodular regenerative hyperplasia
- COMMON FACTOR: focal or diffuse alterations in hepatic blood supply, arising from:
1. Obliteration of portal vein radicles, and
2. Compensatory augmentation of arterial blood supply - NOTE: FNH doesn’t have much clinical significance vs. NRH, which can cause portal HTN
57
Q
What is this?
A
- Focal nodular hyperplasia: broad fibrous scar with hepatic arterial and bile duct elements
- Chronic inflammation in parenchyma lacking normal architecture due to hepatocyte regeneration
- A little bit of duct hyperplasia: reactive process
58
Q
What do you see here?
A
Focal nodular hyperplasia: all bile ducts in the fibrous area with inflammation
59
Q
What is this? Describe the condition.
A
- Nodular regenerative hyperplasia: trichrome highlights compressed central veins
- Denotes liver entirely transformed into nodules: grossly similar to micronodular cirrhosis, but w/o fibrosis
- Can lead to devo of portal HTN
- Association with conditions affecting intrahepatic blood flow, incl. solid-organ (esp. renal) transplant, hematopoetic stem cell transplant, and vasculitis
- Usually incidental finding
60
Q
What is going on in these 2 images?
A
- Nodular regenerative hyperplasia: gross (left) and cut (right) appearance
- May resemble cirrhosis grossly
- Nodules less well-defined in the cut appearance; parenchyma softer than in cirrhosis, and fibrous septa lacking
61
Q
What do you see here?
A
-
Nodular regenerative hyperplasia: nodule in the center of the field in which plates in center of the field are wide, and plates at the edge are narrowed
1. This change, in the absence of significant fibrosis, is indicative of nodular regenerative hyperplasia
2. Silver stain highlights reticulin framework of liver: can be difficult to see this w/o this stain - Normally liver cell plates (lined by dark-staining reticulin fibers) should be of equal width -> 1 hepatocyte wide
- Sinusoids full of proteinaceous material
- NO inflammation, unlike FNH
62
Q
What is this?
A
- Nodular regenerative hyperplasia: micro plump hepatocytes surrounded by rims of atrophic hepatocytes
- Sinusoidal dilation present (arrows); filled with proteinaceous material
- No inflammatory infiltrate or areas of necrosis
63
Q
What is going on here?
A
- Nodular regenerative hyperplasia: reticulin staining highlights characteristic pattern of atrophic hepatic cords (left) and plump, thickened cords (right)
64
Q
What is this? Gross appearance?
A
- Cavernous hemangioma: BENIGN blood vessel tumors identical to those occurring elsewhere
- MOST COMMON benign liver tumors
- HISTO: blood-filled vascular channels (dilated vessels) separated by a dense, fibrous stroma
- GROSS: discrete, red-blue, soft nodules, usually <2cm in diameter, and generally located directly beneath the capsule, so prone to rupture, making them clinically significant
1. NUTMEG color: alternating light and dark colors -> means there is congestion
65
Q
What do you see here? Characteristic histo?
A
- Hepatocellular adenoma: benign, and devo from hepatocytes -> both oral contraceptives (OC’s) and anabolic steroids are assoc w/devo of these
- Incidental, or can cause pain w/rapid growth; rather well-circumscribed
- Rupture is a surgical emergency
- HISTO: cords of hepatocytes with an arterial vascular supply (arrow), and NO PORTAL TRACTS
66
Q
What should this make you think?
A
- Hepatocellular adenoma: cords of hepatocytes, with an arterial vascular supply (arrow) and no portal tracts
68
Q
What is this?
A
- Hepatoblastoma: most common liver tumor of early childhood (<3-y/o), and resemble fetal liver
- Can be epithelial or mixed with mesenchymal elements (osteoid (favorable), cartilage)
- Frequent activation of WNT pathway: association with APC/Familial adenomatous polyposis (FAP)
1. Also associated with Beckwith-Wiedemann (overgrowth disorder) and hemi-hypertrophy - Fatal if untreated; sx + chemo = 80% 5-yr survival
- Variable clinical presentation
69
Q
What do you see here? Gross appearance?
A
- Hepatoblastoma: normal liver on the left, and abnormal on right with a pseudopapillary look
- See attached gross appearance
70
Q
What is going on here? Describe the disease, gross, and micro.
A
- Hepatocellular carcinoma (HCC): high assoc with Hep B and Hep C, chronic liver disease
- Cirrhosis NOT mandatory for hepatocarcinognesis
- Also seen with aflatoxin (Aspergillus) and alcohol
1. Synergistic effect - Activation of β-catenin and inactivation of p53 are the two most common early mutational events
- More common in MALES (5th most deadly cancer)
- INC alpha fetal protein (50%) b/c liver can make this
- GROSS: yellow-tan, kind of nodular appearance; even outside liver appears a little abnormal and nodular here
- MICRO: if well-differentiated, can look almost exactly like normal liver
1. Degenerating hepatocyte in bottom image
71
Q
Compare the progressive stages of HCC and cholangiocarcinoma in terms of: focality in liver, pre-malignancy, assoc w/cirrhosis, and other commonly associated diseases (table).
A
- Small cell vs. large cell and low-grade vs. high-grade really not that important for us to know
- Wouldn’t spend too much time on this chart…
72
Q
What is this?
A
- Fibrolamellar variant of HCC:
- 85% occur under age 35-y/o, and w/o gender predilection or identifiable pre-disposing conditions
1. Kids, but older than hepatoblastoma - Malignant hepatocytes in dense, fibrous stroma
1. Can see some cholestasis here too
2. Scarring, fibrotic gross/micro appearance
73
Q
What is this?
A
- Gross appearance of fibrolamellar variant of HCC
- Scarring, fibrotic gross and micro appearance
74
Q
What is going on here? Describe gross and histo.
A
-
Nodule-in-nodule growth in distinctively large nodule of Hep-C-related cirrhosis
1. Suggests an EVOLVING CANCER - HISTO: top half moderately differentiated HCC, and bottom half well-differentiated HCC
1. Moderately differentiated: bigger nuclei, a little more pleomorphic, look for mitotic figures
2. Well-differentiated can be difficult to distinguish from “normal” liver tissue
75
Q
What do you see here?
A
- Cholangiocarcinoma (CCA): 2nd most common 1o malignant liver tumor after HCC -> malignancy of biliary tree, arising from bile ducts w/in and outside the liver
- Perineural invasion in image on the right, and desmoplasia in the left image
- All risk factors for CCA cause chronic inflam and cholestasis
- Perihilar tumors = Klatskin tumors (50%)
- Premalignant lesions for CCA are also known, the most important of which are biliary intraepithelial neoplasias (low to high grade, BilIN-1, -2, or -3).
- Associated with liver flukes (infection) such as Opisthorchis and Clonorchi (uncommon in the US)
76
Q
What is this?
A
- Cholangiocarcinoma (CCA): often make MUCIN
- Most well- to moderately-differentiated w/clearly defined glandular/tubular structures lined by malignant epithelial cells
1. Prominent nucleoli: can be a giveaway that this is malignant
2. Not all sitting on BM: moving toward luminal space - Typically incite marked desmoplasia
- Lymphovascular invasion and perineural invasion are both common
78
Q
What is going on here?
A
- Metastases to the liver: involvement of the liver by metastatic malignancy is far more common than primary hepatic neoplasia
- Most common primary sources are the colon, breast, lung, and pancreas
79
Q
What is this?
A
- Cholestasis: systemic retention of bilirubin and other solutes eliminated in the bile
- Caused by impaired bile formation and bile flow that gives rise to accumulation of bile pigment in the hepatic parenchyma
- Can be caused by extrahepatic or intrahepatic obstruction of bile channels, or by defects in hepatocyte bile secretion
81
Q
What is the pathway of bilirubin metabolism?
A
- See attached image for steps 1-3
- Step 4: glucuronidation generates bilirubin monoglucuronides and diglucuronides, which are water soluble and readily excreted into bile
1. Big deal is whether conjugated or not: this distinction will help you discriminate b/t different diseases - Step 5: gut bacteria deconjugate bilirubin and degrade it to colorless urobilinogens
- Step 6: urobilinogens and residue of intact pigments are excreted in the feces, with some reabsorption and excretion into urine
83
Q
In what 2 forms can bilirubin accumulate in the body? Causes?
A
- CONJUGATED: not quite as big a deal, and not as bad for tissue b/c excreted in urine/feces
1. Choledocholithiasis: impaired bile duct flow/obstruction
2. Deficiency of canalicular membrane transporters (Dubin-Johnson syndrome, Rotor syndrome)
1. Impaired bile flow from duct obstruction or autoimmune cholangiopathies - UNCONJUGATED: bigger deal, and can accumulate in tissues -> liver can’t keep up
1. Typically bound to albumin, but small fraction of unbound is the problem
2. Can go into brain, and cause kernicterus, creating yellow color (esp. in kids): physiologic jaundice of newborn -> can’t get rid of heme breakdown products/bilirubin fast enough
3. Excess production of bilirubin: hemolytic anemias, resorption of blood from internal hemorrhage (e.g., alimentary tract bleeding, hematomas), ineffective erythropoiesis (e.g., pernicious anemia, thalassemia)
4. Reduced hepatic uptake: drug interference with membrane carrier systems, some cases of Gilbert syndrome
5. Impaired bilirubin conjugation: physiologic jaundice of the newborn (decreased UGT1A1 activity, decreased excretion), breast milk jaundice (β-glucuronidases in milk), genetic deficiency of UGT1A1 activity (Crigler-Najjar syndrome types I and II), Gilbert syndrome (need add’l insult to know they have it), diffuse hepatocellular disease
84
Q
What 5 inherited disorders can lead to bilirubin accumulation? Describe the inheritance, defect, liver pathology, and clinical course of each (table).
A
- Gilbert: most pts don’t ever know they have this until they have an additional insult
- Dubin-Johnson: black liver -> pigmented, cytoplasmic globules (conjugated bilirubin)
- Rotor: not much clinical significance (babies)
85
Q
What is going on here?
A
- Dubin-Johnson Syndrome: impaired excretion of bilirubin glucuronides b/c canalicular membrane-carrier defect (MRP2: multidrug resistance protein 2 mutation)
- Darkly pigmented cytoplasmic globules in liver: ton of bile within the hepatocytes
- Innocuous clinical course
86
Q
What is the white arrow pointing to? When might you see this?
A
- Bile plug due to cholestasis
- Canaliculi -> canal of Hering -> bile ducts
- Can get cholestasis in hepatocytes, and bile plugs in canaliculi: can cause hepatocyte rupture and necrosis
88
Q
What happened here?
A
- Acute large duct obstruction: marked edema of portal tract stroma (white spaces)
- Ductular reaction with admixed neutrophils at the interface between portal tract and hepatocellular parenchyma (interface inflammation)
- Portal tract: bile ducts
- Interface: space b/t portal tract and hepatocytes
89
Q
What is going on here?
A
-
Ascending cholangitis: ppl with large bile duct obstruction risk bacterial infections of static bile in the biliary tree
1. Enteric orgs like coliforms and enterococci are common culprits (E. coli, Enterococcus) - HISTO: neutros in bile duct epithelial lining, and in lumen -> acute inflammation attacking bile ducts
- GROSS: purulent bile fills and distends bile ducts, and pt can get liver abscess formation
1. Pockets of pus
90
Q
What is this? Symptoms? Tx?
A
- Ascending bacterial cholangitis: bile ductules (arrows) with luminal acute inflammatory cells and hepatocytes with intracellular cholestasis
- This is a a severe case -> may be a little bile duct proliferation: neutros attacking them
- SYMPTOMS: fever, chills, abdominal pain, jaundice
- TX: relief of obstruction and AB’s
91
Q
What happened here?
A
- End-stage biliary cirrhosis: due to chronic biliary obstruction -> note the nodularity (arrow) and bile staining
- Ductular rxns from chronic biliary obstruction initiate periportal fibrosis, eventually leading to hepatic scarring and nodule formation, generating 2o or obstructive biliary cirrhosis
- Dilation of the duct system
92
Q
What is this?
A
-
Biliary cirrhosis: unlike other forms of cirrhosis, nodules of liver cells in biliary cirrhosis are often not round, but irregular, like jigsaw puzzle shapes
1. Haphazard - Compare to “other” forms of cirrhosis attached here -> regenerative nodular: hepatitis C (more regular)
93
Q
What might this be? Describe 3 other characteristic features.
A
- Chronic biliary obstruction: retained bile salts cause enlargement of hepatocytes, and gives them a foamy appearance (large, similar to balloon degeneration)
- Cholestatic features:
1. Feathery degeneration of periportal hepatocytes
2. Cytoplasmic swelling, often w/Mallory-Denk bodies (differ from those in alcohol-induced liver disease and non-alcoholic fatty liver disease by periportal predominance), and
3. Formation of bile infarcts - Bile duct proliferation
94
Q
What is this? Describe 3 other characteristic features.
A
- Chronic biliary obstruction: bile plug with necrosis (aka, bile infarct)
- Necrosis: may just see hepatocyte surrounded by inflammation -> macros coming in to clean up (can be very subtle)
- Cholestatic features:
1. Feathery degeneration of periportal hepatocytes
2. Cytoplasmic swelling, often w/Mallory-Denk bodies (differ from those in alcohol-induced liver disease and non-alcoholic fatty liver disease by periportal predominance), and
3. Retained bile salts cause enlargement of, and give foamy appearance to, hepatocytes
95
Q
What do you see here?
A
- Cholestasis of sepsis: most often in response to circulating microbial products (ducts, and not just canaliculi)
- Most common form is canalicular cholestasis: bile plugs within predominantly centrilobular canaliculi
- DUCTULAR CHOLESTASIS: ominous
1. Dilated canals of Hering; bile ductules at the interface of portal tracts and parenchyma also dilated
2. Contain obvious BILE PLUGS (front image)
3. Not a typical feature of biliary obstruction, but septic shock
96
Q
What is this?
A
-
Primary hepatolithiasis: intrahepatic gallstone formation that leads to:
1. Repeated bouts of ascending cholangitis,
2. Progressive inflammatory destruction of hepatic parenchyma, and
3. Predisposes to biliary neoplasia - FRONT IMAGE: atrophic right hepatic lobe with characteristic findings -> markedly dilated, distorted bile ducts containing large pigment stones + broad areas of collapsed liver parenchyma
97
Q
What is the significance of this finding in a neonate?
A
- Neonatal cholestasis: conjugated bilirubin -> should evoke search for recognizable toxic, metabolic, and/or infectious liver disease
- BILIARY ATRESIA: major cause
- NEONATAL HEPATITIS: variety of disorders causing conjugated hyperbilirubinemia
1. Lobular disarray
2. Apoptosis and necrosis
3. Multinucleated giant hepatocytes
98
Q
What is going on in these two extrahepatic neonatal images?
A
- Biliary atresia (left): complete or partial obstruction of the lumen of the extrahepatic biliary tree within the first 3 months of life
- Salient features include: inflammation & fibrosing stricture of the hepatic or common bile ducts
- NOTE: normal bile duct on the right
99
Q
How do the 2 autoimmune cholangiopathies differe in terms of: age, gender, clinical course, associated conditions, serology, radiology, and duct lesions (table)?
A
- Not uncommon
- PSC: ulcerative colitis, onion-skinning
- KNOW THIS TABLE
100
Q
What is this?
A
- Primary biliary cirrhosis (PBC)
- Autoimmune disease
- Characterized by nonsuppurative, inflammatory destruction of small and medium-sized intrahepatic bile ducts
- Bile duct proliferation with inflammation all around it, but not going too far into hepatic parenchyma
101
Q
What do you see here?
A
- Primary biliary cirrhosis (PBC): lymphocytic inflammation and damage to a medium-sized bile duct in a portal tract (long arrow)
- Poorly-formed GRANULOMA on the right side of the bile duct (curved arrow)
- With inflammatory damage to the bile ducts, further flow of bile fluid distal to the damaged bile duct is impeded, resulting is cholestasis and damage to hepatocytes
102
Q
What is going on here?
A
- Primary biliary cirrhosis (PBC): portal fibrosis with eventual development of cirrhosis in untreated cases is the natural course of the disease
- Trichrome stain shows concentric collagen fibrosis in a portal tract
1. Lympho inflam and damage to a medium-sized bile duct in a portal tract + poorly-formed granuloma on R side of bile duct
103
Q
What are these arrows pointing to? Why is this happening?
A
- Primary biliary cirrhosis (PBC): compensatory bile ductular proliferation (long arrow) in portal tracts proximal to obstructed regions
- Bile ductules: small-caliber ducts with cuboidal to flattened epithelium, often with collapsed lumima
- Presence of multiple bile ductules in the periphery of a portal is a telltale sign of distal bile duct damage in the biliary tree
104
Q
What is this immunostain for? Showing?
A
- Primary biliary cirrhosis (PBC): extent and geography of reactive bile ductular proliferation can be highlighted by immunostaining for CK-7 b/c normal bile ducts are positive for this antigen
- Note the absence of any medium-sized bile ducts inside the portal tract, and a rather brisk bile ductular proliferation at the portal border
- Destruction of normal bile ducts in portal tract, and compensatory INC of bile ducts on the outside
105
Q
What is this?
A
- Regenerative hepatic nodule surrounded by bridging fibrosis
- In this case, primary biliary cirrhosis: with progressive hepatocyte damage and fibrosis, portal-portal bridging fibrosis and frank cirrhosis develop
- Fibrosis is “bridging,” connecting the different portal tracts
106
Q
What is this image characteristic of?
A
- Primary sclerosing cholangitis: characteristic beading on radiographs
- PSC is characterized by inflammation and obliterative fibrosis of intrahepatic and extrahepatic bile ducts with dilation of preserved segments
107
Q
What is this?
A
- Primary sclerosing cholangitis: culminates in biliary cirrhosis much like that seen with chronic obstruction and primary biliary cirrhosis
- LARGE DUCT inflammation: acute, neutrophilic infiltration of the epithelium superimposed on a chronic inflammation
- SMALL DUCT: little inflammation and a striking circumferential “onion skin” fibrosis around atrophic duct lumen, with eventual obliteration
- Biliary intraepithelial neoplasia may develop and cholangiocarcinoma -> usually w/fatal outcomes
108
Q
What do you see here?
A
- Primary sclerosing cholangitis: degenerating bile duct with “onion skin” fibrosis
- Cholestasis
- Biliary cirrhosis
110
Q
What is this? Presentation? Risks?
A
- Choledochal cyst: congenital dilation of common bile duct
- PRESENTATION: kids before age 10 with jaundice and/or recurrent abdominal pain, and symptoms typical of biliary colic
1. F:M ratio 3:1-4:1 - Occur in conjunction w/cystic dilation of intra-hepatic biliary tree (Caroli disease) in some cases
- Predispose to stone formation, stenosis/stricture, pancreatitis, and obstructive biliary complications within the liver
1. In older pts, risk of bile duct carcinoma is elevated
111
Q
What is going on here?
A
- Von Meyenburg complexes: bile duct hamartoma always associated with portal tracts
- Dilated and irregularly shaped bile ducts in fibrous background stroma
-
Fibropolycystic disease of liver: heterogeneous group of lesions in which the primary abnormalities are congenital malformations of the biliary tree
1. INC risk for cholangiocarcinoma - Can be confused with neoplasms, so often sent to pathology
112
Q
What happened here?
A
- Single, or multiple (front), intra- or extrahepatic (i.e., along bile tract, or in liver) biliary cysts: when present in isolation, these may be symptomatic due to ascending cholangitis
1. Caroli disease - CAROLI SYNDROME (front): when biliary cysts occur along w/congenital hepatic fibrosis
1. Ducts may be cystically dilated, but true cysts are also present -> may be intrahepatic cysts or choledochal cysts -
Fibropolycystic disease of liver: heterogeneous group of lesions in which the primary abnormalities are congenital malformations of the biliary tree
1. INC risk for cholangiocarcinoma
113
Q
What is this?
A
- Congenital hepatic fibrosis: portal tracts are enlarged by irregular, broad bands of collagenous tissue, forming septa that divide the liver into irregular islands
- Auto recessive: linked w/muts in PKHD1 gene on chrom 6, leading to ductal plate malformation of intralobular bile ducts
-
Not truly cirrhotic, despite serpiginous scarring separating the hepatic parenchyma, BUT may still face complications of portal HTN, particularly bleeding varices
1. Looks like von Meyenburg histologically, but V-M will NOT get these manifestations
114
Q
What is going on here?
A
- Congenital hepatic fibrosis: variable numbers of abnormally shaped bile ducts are embedded in the fibrous tissue, although they remain in continuity with the biliary tree
115
Q
What happened here? Manifestations? Causes?
A
- Budd-Chiari Syndrome: portal HTN due to thrombosis of hepatic veins
- Severe centrilobular congestion/necrosis, progressing to centrilobular fibrosis (hard to see necrosis in front image b/c acute, and inflam hasn’t moved in yet)
- Acute: can be fatal
- MANIFESTATIONS: hepatomegaly, abdominal pain, ascites
- CAUSES: polycythemia vera/myeloproliferative diseases, pregnancy, oral contraceptives (OC), abdominal cancer (esp. in the liver)
118
Q
What do you see here?
A
- Preeclampsia: periportal sinusoids contain fibrin deposits associated with hemorrhage into SPACE of DISSE
- Can lead to periportal hepatocellular coagulative necrosis (see attached image)
119
Q
What happened here?
A
- Eclampsia: blood under pressure may coalesce and expand to form a hepatic hematoma
- Dissection of blood under Glisson capsule may lead to catastrophic hepatic rupture in eclampsia
1. Medical emergency
121
Q
What is this?
A
- Acute fatty liver of pregnancy: microvesicular steatosis in zones 2 or 3 (vacuoles may be very sm)
- Also marked ballooning of hepatocytes and macrovesicular fat
- In severe cases, hepatocyte dropout, reticulin collapse, portal tract inflammation
122
Q
What is this?
A
- Intrahepatic cholestasis of pregnancy: 2nd leading cause of gestational jaundice (after viral hepatitis) -> usually occurs late in pregnancy
- Estrogenic hormones may INH hepatocellular bile secretory activity
- Mother at-risk for gallstones, malabsorption
- Associated with higher incidence of fetal distress, stillbirths, prematurity
- SYMPTOMS: pruritis in third trimester, dark urine, light stools, jaundice
- LABORATORY: some may have elevated serum bilirubin (< 5 mg/dl), usually conjugated; mildly elevated alkaline phosphatase
123
Q
What is going on here?
A
- Gaucher disease: genetic metabolic disorder in which glucocerebroside (a sphingolipid, also known as, glucosylceramide) accumulates in cells and certain organs
- Most common lysosomal storage disease
- A few types, but type 1 most common
- Enlarged liver and spleen -> if bone marrow involved, trilineage decrease
- CRINKLED PAPER APPEARANCE (tissue paper)
124
Q
What do you see here?
A
-
Normal liver: reticular fibers black with silver, and nuclei red with nuclear fast red
1. Hepatocyte plates just 1-2 cells; pattern of reticulin can show you regenerative nodules and parenchymal collapse - Well-differentiated HCC will lose reticulin (see attached image: malignant cells have lost reticulin)
126
Q
What is going on in each of these livers?
A
- Healthy
- Fatty: note the differences b/t normal and fatty liver attached here too
- Cirrhosis
- NOTE: hepatocytes can undergo a # of degenerative, but potentially reversible changes, like accumulation of fat (steatosis) and bilirubin (cholestasis)
127
Q
What pathology do you see here?
A
- Fatty liver = steatosis
128
Q
What is this?
A
- Bilirubin = cholestasis
129
Q
What is this? Arrows?
A
- Hepatocyte necrosis: osmotic regulation -> fluid flows into the cell, which swells and ruptures
- Macros clean up
- Predominant mode of death is ischemic/hypoxic injury and a significant part of the response to oxidative stress
- Spotty necrosis: normal liver cells surrounding group of macros cleaning up dead hepatocytes (not going to see confluent necrosis often b/c no reason to biopsy these pts)
130
Q
What do you see here?
A
-
Hepatocyte apoptosis: active form of “programmed” cell death resulting in:
1. Hepatocyte shrinkage,
2. Nuclear chromatin condensation (pyknosis),
3. Fragmentation (karyorrhexis), and
4. Cellular fragmentation into acidophilic apoptotic bodies (aka, Councilman bodies; acidophil bodies) - Eosinophilic
131
Q
What is this?
A
- Confluent necrosis: widespread parenchymal loss with loss of reticular structures b/t hepatocytes
- Zones matter
- HISTO: cellular debris, macros, and remnants of the reticulin meshwork
132
Q
What do you see here?
A
- Bridging necrosis: zone that may link central veins to portal tracts or bridge adjacent portal tracts
- Areas of necrosis starting to connect BEFORE you get to confluent necrosis
- In some cases, there is scar regression
133
Q
How does liver regeneration work?
A
- Primarily via mitotic replication of hepatocytes adjacent to those that have died, even when there is significant confluent necrosis
- Hepatocytes almost stem cell-like in their ability to continue to replicate even in the setting of years of chronic injury, and thus stem cell replenishment is usually not a significant part of parenchymal repair
134
Q
What is the principal cell type involved in scar deposition in the liver?
A
- Stellate cell: in its quiescent form, it is a lipid (vitamin A) storing cell, but in several forms of acute and chronic injury, these can become activated and are converted into highly fibrogenic myofibroblasts
- When activated, they are a major player in fibrosis and scarring (aka, cells of Ito)
135
Q
How does scar formation and regression occur in the liver?
A
- Kupffer cell activation leads to secretion of multiple cytokines
1. PDGF and TNF activate stellate cells - Contraction of activated stellate cells is stimulated by endothelin-1 (ET-1)
- Fibrosis is stimulated by TGF-β
- Chemotaxis of activated stellate cells to areas of injury is promoted by PDGF and monocyte chemotactic protein-1 (MCP-1)
136
Q
What is this?
A
- Liver cirrhosis: zones of parenchymal loss transform into dense fibrous septa -> combo of the collapse of underlying reticulin where lg swaths of hepatocytes have irrevocably disappeared and hepatic stellate cells have been activated
- Eventually, these fibrous septa encircle surviving, regenerating hepatocytes in the late stages of chronic liver diseases that give rise to diffuse scarring described as cirrhosis
- Looks different than biliary cirrhosis, which has more of a jigsaw look
- This example is likely from something like Hep C
138
Q
Which zone has the lowest O2 and nutrient supplies?
A
- Zone 3: this zone is very susceptible to anoxic, toxic and nutritional injury
139
Q
What is going on here?
A
- Acute hepatic necrosis: portal areas show inflam, most likely related to preexisting alcoholic liver disease; hepatocytes mostly viable, but an edge the necrotic zone is apparent (arrows)
- Attached image: here the zonal necrosis is present around three central veins (V), while hepatocytes near portal areas (P) remain viable (massive acute necrosis)
- Drugs are big players here
140
Q
What happened here?
A
- Acute (sudden and massive) hepatic necrosis: liver is small, bile-stained, soft, and congested
- Hepatocellular necrosis caused by acetaminophen overdose
- IMAGE: zonal necrosis present around central vein (arrow/zone 3), while hepatocytes near portal areas (asterisk) remain viable
141
Q
What is this?
A
- Diffuse microvesicular steatosis: diffuse poisoning of liver cells w/o obvious cell death and parenchymal collapse
- Not much known regarding pathogenesis of microvesicular steatosis, but primary defect could be a mitochondrial lesion, and INH of the mitochondrial beta oxidation of fatty acids has been the most frequently implicated defect
- EXAMPLES: fatty liver of pregnancy, idiosyncratic reactions to toxins, but now known to be seen in a large variety of diseases
142
Q
Blue arrow vs. green arrow?
A
- BLUE: microvesicular
- GREEN: macrovesicular
- Typically a mixture of micro- and macro
143
Q
What happened to this guy?
A
- Chronic liver failure: depressed areas of dense scar separating bulging regenerative nodules over the liver surface
- Years/decades of insidious, progressive injury
- CAUSES: chronic Hep B/C, non-alcoholic fatty liver disease, and alcoholic liver disease
- Liver failure in chronic liver disease is most often associated with cirrhosis
1. While cirrhosis implies presence of severe chronic disease, it is not a specific diagnosis and it lacks clear prognostic implications - Cirrhosis diffuse and is comprised of regenerating parenchymal nodules surrounded by dense bands of scar
- A lot of changes in the liver are not specific: need to have the clinical information too
144
Q
What happened here?
A
- Regression of fibrosis: does occur, even in fully established cirrhosis; this is another reason why cirrhosis should not be automatically equated with end stage disease
- Scars can become thinner, more densely compacted, eventually fragment -> fibrous septa break apart, and adjacent nodules of regenerating parenchyma coalesce into larger islands
- IMAGE: alcoholic cirrhosis in an active drinker (A) and following long-term abstinence (B). A, Thick bands of collagen separate rounded cirrhotic nodules. B, After a year of abstinence, most scars are gone. (Masson trichrome stain)
145
Q
What are these?
A
- Hep B ground glass hepatocytes
- Attached image is typically used for Hep B and C
- Mononuclear infiltrate around portal tract: hepatitis -> don’t forget this
- Can get balloon degeneration and spotty necrosis
146
Q
What is this?
A
- Balloon degeneration: can see this with hepatitis
147
Q
Note this grading system for chronic hepatitis.
A
And this staging system for chronic hepatitis.
F0 no fibrosis
F1 portal fibrosis w/o septa
F2 portal fibrosis with few septa
F3 numerous septa w/o cirrhosis
F4 cirrhosis
Good job!
148
Q
What is going on here?
A
-
Autoimmune hepatitis: chronic, progressive hepatitis w/all the features of autoimmune diseases in general:
1. Genetic predisposition
2. Association w/other autoimmune diseases
3. Presence of autoantibodies, and
4. Therapeutic response to immunosuppression - PLASMA CELLS are prominent and characteristic component
- INTERFACE (leaking out of portal tract, basically) hepatitis with plasma cells
