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Pathology Winter Exam 2 > Exam 2 LO > Flashcards

Exam 2 LO Flashcards

1
Q

Define Lymphadenopathy

A

Enlarged lymph nodes (> 1 cm, but really up to interpretation tbh)

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2
Q

Enumerate the 3 general categories causal of node enlargements

A
  • Lymphadenitis (enlargement due to infection/inflammation)
  • Lymphoma (neoplastic proliferation of cells)
  • Metastatic malignancy
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3
Q

Explain the difference between localized & generalized lymphadenopathy

A

Localized lymphadenopathy is when one set of lymph nodes are enlarged. Generalized is when multiple sets are enlarged. If generalized, you need to do a prompt workup to determine the cause.

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4
Q

Describe the circumstances under which an excisional node biopsy may be appropriate

A

If generalized or localized lymphadenopathy is unexplained and persistent beyond 3-4 weeks.

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5
Q

Name the 3 major causes/categories of benign lymphadenopathy

A
  • Infection
  • Inflammatory/autoimmune
  • Drugs (medications like Dilantin)
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6
Q

Recall common etiologies for each of the 8 histologic/pathologic morphologic patterns of benign adenopathy

A
  • Acute suppurative/necrotizing: usually bacterial infection
  • Necrotizing granulomatous lymphadenitis: cat-scratch, tularemia, LGV
  • Follicular hyperplasia: usually due to virus/drug/inflammation, but highlighted early HIV
  • Interfollicular/paracortical hyperplasia: viral (EBV) and SLE
  • Granulomatous lymphadenitis: caseating and noncaseating granulomas (TB, Crohn’s, sarcoidosis, fungi, etc.)
  • Sinus Histiocytosis: common in nodes that are draining carcinomas
  • Mixed Hyperplasia: toxoplasmosis
  • Dermatopathic adenopathy: chronically inflamed skin

Mnemonic:
“A Nurse Found Interesting Medical Groups Studying Dermatology”

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7
Q

Describe the major clinical & laboratory findings of Hemophagocytic Lymphohistiocytosis

A

reactive condition d/t systemic activation of macrophages & cytotoxic T-cells
Clinical:
* Febrile illness
* HSM
* LAD
Labs:
* cytopenias (>2 cell lines)
* hypertriglyceridemia & increased liver enzymes
* increased serum ferritin
* increased soluble CD25
* hypofibrinogenemia (+/- DIC)
* BM: hemophagocytosis

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8
Q

Discuss the commonalities and differences of leukemia vs lymphoma

A
  • Leukemia: widespread BM involvement (usually in peripheral blood)
  • Lymphoma: discrete tissue masses (usually lymph nodes, but can be extra-nodal)
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9
Q

Describe the proper handling and appropriate studies to be performed on excised nodal tissue to enable correct Dx

A
  • Put a sample of fresh tissue in a sterile way to send for culture/analysis
  • Put a sample in transport media for flow cytometry/cytogenetic analysis/FISH/molecular genetic analysis
  • Fix the tissue using formalin for histology and immunohistochemistry analyses
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10
Q

Explain how Clonality is determined for B and T Lymphoid neoplasms

A
  • B cells: surface Ig with K or L light chain restriction by Flow Cytometry
  • T cells: clonal T cell receptor (TCR) gene rearrangements by PCR
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11
Q

Recall normal B-cell development in the normal follicle

A
  • Progenitor lymphoid B cell
  • Naive B cell
  • Mantle zone
  • Centroblast (clonal expansion)
  • Centrocyte
  • Plasmablast or memory B cell in the marginal zone
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12
Q

For Follicular lymphoma, recall the translocation & what is overexpressed

A
  • Translocation: t(14;18)
  • Increasing BCL2 expression (decreasing apoptosis)
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13
Q

Name the most common type of NHL

A

DLBCL (diffuse large B cell lymphoma)

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14
Q

For DLBCL describe its behavior, name 2 common mutations, describe features of clinical presentation and special types

A
  • Aggressive
  • Common mutations: BCL6 and BCL2
  • Clinically: can be extranodal ⅓ of the time - often in Waldeyer ring (oropharynx lymphoid tissue)
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15
Q

For Burkitt lymphoma, discuss its clinical features and defining genetic feature

A
  • Highly aggressive lymphoma
  • children or young adults
  • Most are extranodal
  • often latently infected w/ EBV
  • Upregulation of Myc gene due to t(8;14) translocation
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16
Q

For Mantle cell lymphoma recall: cell of origin, translocation, resulting upregulation

A
  • Originates in naive B cells
  • Upregulation of Cyclin D1
  • Translocation: t(11;14)
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17
Q

For Marginal Zone Lymphoma/MALToma name common contextual background diseases

A
  • Sjogren syndrome
  • Hashimoto Thyroiditis
  • H. pylori gastritis
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18
Q

C/C mature peripheral T/NK cell lymphomas with B-cell lymphomas

A
  • Uncommon
  • Worse prognosis
  • Originate from T cells
  • Hard to diagnose
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19
Q

Name the most common type of mature T-cell lymphoma

A

Peripheral T-cell Lymphoma, unspecified
*worse Px than B-cell Lymphomas

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20
Q

Name, for Anaplastic Large cell lymphoma the IHC marker

A
  • CD30 (Ki-1) IHC marker
  • T-cell tumor - NHL
  • ALK - Anaplastic Lymphoma Kinase translocation

involves nodal & extranodal sites, often skin

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21
Q

Name the most common cutaneous T-cell lymphoma

A

Mycosis Fungoides/Sezary syndrome

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22
Q

Name cell of origin for MF/Sezary syndrome

A

CD4+ Th cell

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23
Q

What are the 3 clinical stages of Mycosis Fungoides?

A
  • Patch
  • Plaque
  • Tumor
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24
Q

What defines Sezary Syndrome

A

Erythroderma + circulating malignant T-cells (Leukemia of “Sezary” cells)
* Sezary cell with characteristic hyperconvoluted, “cerebriform” nucleus

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25
Q

Elucidate the salient features of Extranodal NK/T cell lymphoma

A

*Formerly - Lethal Midline Granuloma
* nasopharynx in midline
* tumor cells surround & invade vessels leading to ischemic necrosis
* EBV etiology
* NK cell origin

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26
Q

For HL, what are the 4 classical subtypes?

A
  • Nodular Sclerosis
  • Mixed Cellularity
  • Lymphocyte Rich
  • Lymphocyte Depletion
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27
Q

What is the malignant cell that defines HL?

A

Reed-Sternberg cell

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28
Q

What are common presenting signs/symptoms of HL?

A
  • Nontender adenopathy in a single or group of axial nodes
    1. cervical neck nodes > half
    2. mediastinal nodes > half
  • initially: spread predictably to contiguous node groups
  • late: spread to liver, spleen & finally BM and other tissues
  • Pel-Ebstein fever (cyclic fever over 1-2 week intervals)
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29
Q

What are ‘B symptoms’? A symptoms?

A

B symptoms: fevers, night sweats, weight loss. If absent, they are A symptoms.

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30
Q

Be able to identify classic R-S cells

A

Diagnostic R-S cells:
* large Binucleated/bilobed nucleus - “mirror image nuclei” with prominent eosinophilic nucleoli (owl’s eyes)
Nodular Sclerosis (NS) subtype:
* Lacunar R-S variants
* MC mononuclear variants
R-S cells & Classical HL:
* CD15+
* CD30+

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31
Q

Be able to Stage HL

A

Ann Arbor Staging:
Stage I: single lymph node region or single extralymphatic site
Stage II: two or more lymph node regions on same side of diagraphm
Stage III: lymph nodes on both sides of diaphragm
Stage IV: diffuse extralymphatic disease (e.g. in liver, bone marrow, lung, skin)

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32
Q

The salient features of Nodular Sclerosis Type

A
  • Most common
  • Prognosis excellent
  • Young adults and adolescents
  • Mediastinum usually involved
  • EBV negative
  • Histology
    1. collagen bands form nodules
    2. lacunar RS cells present
  • CD15+, CD30+
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33
Q

For Thymus, be aware of the Thymic Follicular Hyperplasia & Thymoma connection with Myasthenia Gravis

A

If you see thymic hyperplasia, you either have myasthenia gravis or Graves disease.

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34
Q

What is the risk period for CMV & Rubella?

A

First trimester (specifically weeks 3-9, but 4-5 are the MOST RISKY)

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35
Q

What is a common cause of first trimester fetal loss?

A

Genetic causes

Congenital infections are often seen as fetal loss later in pregnancy.

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36
Q

What are the fetal defects associated with CMV infection?

A
  • Microcephaly
  • Deafness
  • Chorioretinitis
  • Hepatosplenomegaly
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37
Q

What are the fetal defects associated with Rubella infection?

A
  • Congenital cataracts
  • Cardiac defects (PDA)
  • Microcephaly
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38
Q

What are the features of fetal alcohol syndrome?

A
  • Microcephaly
  • Short palpebral fissures
  • Maxillary hypoplasia
  • Thin upper lip
  • Low bridge nose
  • Frontal bossing
  • Mentally handicapped
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39
Q

When is the highest risk period for alcohol consumption during pregnancy?

A

First trimester

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40
Q

What are the features of retinoic acid embryopathy?

A
  • CNS defects
  • Cardiac defects
  • Craniofacial defects (cleft palate)
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41
Q

What is a common consequence of nicotine smoking during pregnancy?

A
  • Low birth weight
  • Increased risk of SIDS
  • High incidence of fetal loss and stillbirth
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42
Q

What are the features of diabetic embryopathy?

A
  • Cardiac anomalies
  • Neural tube defects
  • Kidney, gut, and skeletal system anomalies
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43
Q

What is fetal macrosomia and what is it associated with?

A

Increased body fat and muscle mass with organomegaly; usually due to maternal hyperglycemia

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44
Q

What is the most susceptible period for teratogens during intrauterine development?

A

Weeks 3-9

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45
Q

What do the terms AGA, SGA, and LGA stand for?

A
  • AGA: Appropriate for gestational age
  • SGA: Small for gestational age
  • LGA: Large for gestational age
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46
Q

What is the definition of prematurity?

A

Any birth before 37 weeks gestation

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47
Q

What are the major risk factors for prematurity?

A
  • PROM - premature rupture of membrane
  • Intrauterine infections
  • Uterine/cervical/placental abnormalities
  • Multiple gestations
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48
Q

What does FGR stand for?

A

Fetal Growth Restriction

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49
Q

What are the three main groups of factors causing FGR?

A
  • Fetal factors
  • Placental factors
  • Maternal factors
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50
Q

What is another term for respiratory distress syndrome?

A

Neonatal respiratory distress syndrome (hyaline membrane disease)

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51
Q

What is the primary deficiency in RDS?

A

Pulmonary surfactant

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52
Q

What are the characteristics of an infant with RDS?

A
  • Usually preterm
  • weight AGA
  • Associated with male sex
  • maternal diabetes
  • C-section delivery
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53
Q

What are the clinical symptoms of necrotizing enterocolitis?

A
  • Bloody stools
  • Abdominal distention
  • Hypotension
  • Circulatory collapse
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54
Q

What does TORCH stand for?

A
  • Toxoplasmosis
  • Other (syphilis, hepatitis, HIV)
  • Rubella
  • CMV
  • Herpes simplex
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55
Q

What is the classic deficiency in PKU?

A

Phenylalanine hydroxylase (PAH) enzyme

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56
Q

What is the consequence of the deficiency in PKU?

A

Accumulation of phenylalanine and its metabolites

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57
Q

What odor is associated with infants who have PKU?

A

Strong mousy or musty odor

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58
Q

What is the most common variant of galactosemia lacking?

A

GALT (galactose-1-phosphate uridyl transferase) enzyme

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59
Q

What accumulates in the tissues in the common variant of galactosemia?

A

Galactose-1-phosphate

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60
Q

What is the fundamental defect in cystic fibrosis?

A

Defect in CFTR gene

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61
Q

What does the CFTR gene code for?

A

Epithelial chloride channel

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62
Q

What are the major clinical features of classic cystic fibrosis?

A
  • Recurrent lung infections
  • Pancreatic insufficiency
  • Intestinal blockage
  • Liver abnormalities
  • Male genital tract abnormalities
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63
Q

What happens to the submucosal glands in the lungs in cystic fibrosis?

A

Secrete viscous mucus, leading to obstruction and secondary infection

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64
Q

What is the single most common cause of death in cystic fibrosis?

A

Complications from recurrent lung infections

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65
Q

What does SIDS stand for?

A

Sudden Infant Death Syndrome

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66
Q

What is ALTE?

A

Apparent life-threatening event

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67
Q

What is the most common nonspecific finding at autopsy in SIDS?

A

Petechiae on the thymus, pleura, and pericardium

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68
Q

What are the three factors of the triple risk hypothesis?

A
  • Vulnerable infant
  • Critical development period
  • Environmental causes
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69
Q

What is Sister Mary Joseph nodule?

A

Metastatic cancer to the umbilicus
Common mets from:
* gastric cancer
* colon cancer
* pancreatic cancer
* ovarian cancer

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70
Q

What is Virchow’s node?

A

Left supraclavicular lymph node at the junction of the thoracic duct and left subclavian vein

associated with gastric malignancy

Indicative of metastatic gastric carcinoma

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71
Q

Define Bezoars.

A

Tightly packed collection of undigested material in the stomach

Can lead to obstruction

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72
Q

What are gastric diverticula?

A

Outpouchings of the stomach wall; can be congenital or acquired

True diverticula contain all layers; false ones only have mucosa and submucosa

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73
Q

What is gastric volvulus?

A

Twisting of the stomach, considered a surgical emergency

Classic triad: severe epigastric pain, retching without vomiting, inability to pass NG tube

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74
Q

What is atresia?

A

Absence or complete narrowing of a passage

Most commonly seen as an imperforate anus

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75
Q

Define stenosis.

A

Narrowing of a lumen

Can occur in various organs

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76
Q

What is a fistula?

A

Abnormal passage between two organs or an organ and the exterior body

Commonly a tracheoesophageal fistula

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77
Q

What does ectopia/heterotopia/developmental rests mean?

A

normal tissue located outside of their normal place or organ

Considered a ‘stranger in a strange land’

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78
Q

Define hernia.

A

Displacement of an organ through the wall of its cavity

Usually occurs through a weak point

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79
Q

What is a diverticulum?

A

Blind outpouching of the wall of an organ with a lumen

Can occur in various organs, including the stomach

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80
Q

What is an adhesion?

A

Scar tissue that connects anatomical structures not usually connected

Can cause complications like obstruction

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81
Q

What is a viscus?

A

Any hollow organ inside a large body cavity
esp. the hollow organs in the abdominal cavity

Examples include the stomach and intestines

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82
Q

Define ulcer.

A

Denudation of an epithelium -
loss of skin or mucous membrane epithelial covering with acute & chronic inflammation & attempts at repair of the exposed underlying connective tissue

Characterized by repair attempts at the site

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83
Q

What is erosion?

A

Superficial ulcer without muscularis mucosa penetration

A less severe form of ulceration

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84
Q

Define intussusception.

A

Proximal part of intestine invaginating into distal portion

Can lead to obstruction and is a surgical emergency

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85
Q

What is volvulus?

A

Twisting of intestine around its mesenteric attachment site

Can occur in various parts of the gastrointestinal tract

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86
Q

What is omphalocele?

A

Midline abdominal defect with herniation of abdominal contents into a sac

Usually associated with birth defects

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87
Q

What is gastroschisis?

A

Abdominal wall defect to the right of the umbilical cord without a sac
no parietal peritoneal covering extruded bowel

Typically occurs in isolation without associated defects

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88
Q

What is diaphragmatic hernia?

A

Failure of diaphragm to close completely during development, leading to herniation of abdominal contents into the chest leading to:
Pulmonary hypoplasia

Life threatening - Surgical correction is necessary

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89
Q

What is an Inlet Patch?

A

Gastric mucosa in the upper 1/3 of the esophagus

Usually asymptomatic but can lead to complications

90
Q

What is Meckel Diverticulum?

A

Diverticulum from the vitelline (omphalomesenteric) duct that persists
which connects fetal gut to yolk sac

Located on the anti-mesenteric side of the distal ileum

91
Q

What is the Rule of 2’s in Meckel Diverticulum?

A
  • 2% prevalence
  • 2 feet from ileocecal valve
  • 2 inches long
  • 2x common in males
  • often symptomatic by age 2
92
Q

What is hypertrophic pyloric stenosis?

A

Condition presenting in infants with projectile vomiting due to hyperplasia of pyloric muscularis propria

  • common 1/250 caucasian births
  • 4X common in boys
  • present weeks 2-5 of life with projectile vomiting
  • Thick pylorus may present as mid-abdominal mass

Surgical intervention is required

93
Q

What is Hirschsprung Disease?

A

Congenital - segmental absence of ganglion cells (aganglionosis) leading to intestinal obstruction

sustained contraction of involved segment with functional obstruction

Characterized by failure to pass meconium

94
Q

What is acute gastritis?

A

Inflammatory condition of the gastric mucosa associated with acute stress

uclers - usually multiple, superficial & located in acid producing mucosa (fundus/body)

c/c with chronic PUD which are single, deeply penetrating & usually located in the duodenum or lesser curvature of antrum

95
Q

Define gastropathy.

A

Pathologic condition of the gastric mucosa with minimal inflammation

Different from gastritis, which has inflammatory cells

96
Q

What do parietal cells secrete?

A

HCl and intrinsic factor

Intrinsic factor is essential for vitamin B12 absorption

97
Q

What is the function of chief cells?

A

Secrete pepsinogen

Pepsinogen is activated to pepsin in acidic conditions

98
Q

What do G cells secrete?

A

Gastrin and histamine

Both of which increase HCl secretion

99
Q

What is the role of delta cells?

A

Secrete somatostatin

Somatostatin decreases HCl secretion

100
Q

What do ECL cells secrete?

A

Histamine

Histamine increases HCl secretion

101
Q

What is the key protein for gastric acid secretion?

A

Proton pump (H+/K+ ATPase)

Located on parietal cells

102
Q

What are stress ulcers?

A

Ulcers caused by severe physiological stress, shock, or trauma

Include Curling ulcers (burns) and Cushing’s ulcers (intracranial disease)

103
Q

What is Menetrier Disease?

A

Hypoproteinemic hypertrophic gastropathy characterized by foveolar hyperplasia

Increases risk of gastric adenocarcinoma

104
Q

What is Zollinger-Ellison syndrome (Z-E syndrome)?

A

Gastrin-secreting tumors causing increased acid production

Can lead to duodenal ulcers

105
Q

What is Dieulafoy’s lesion?

A

Aberrant dilated submucosal blood vessel that erodes epithelium

Can cause upper GI bleeding

106
Q

What is GAVE?

A

Gastric antral vascular ectasia, also known as watermelon stomach (antrum)

Characterized by dilated capillaries in the lamina propria with fibrin thrombi

107
Q

What are the two types of chronic gastritis?

A

H. pylori associated and autoimmune gastritis

Each has different pathologies and complications

108
Q

What is atrophic gastritis?

A

Metaplastic Atrophic Gastritis (MAG)
Thinning & replacement of the native gastric mucosa by* intestinal metaplastic* mucosa (atrophy)

Two Subtypes:
1. Autoimmune (A-MAG)
2. Environmental (EMAG)

Associated with increased risk of gastric cancer

109
Q

What are the common causes of peptic ulcer disease (PUD)?

A

H. pylori, NSAIDs, cigarette smoking, stress, genetics

Caused by an imbalance between defense and injury

110
Q

What is Milk-Alkali syndrome?

A

Condition caused by excessive calcium leading to hypercalcemia

Can cause kidney failure and metabolic alkalosis

111
Q

What are the three most common types of gastric polyps?

A
  1. Hyperlastic/Inflammatory
  2. Fundic Gland
  3. Adenomatous

Adenomatous polyps are pre-malignant

112
Q

What are the two clinicopathologic types of gastric adenocarcinoma?

A
  1. Intestinal type (most common)
  2. Diffuse type

Each has distinct morphologic and molecular features

113
Q

What is a Krukenberg tumor?

A

Bilateral metastatic cancer to the ovaries from gastric adenocarcinoma

Typically associated with signet ring cell type

114
Q

What is a carcinoid tumor?

A

Well-differentiated neuroendocrine tumor derived from enterochromaffin or ECL cells

Can secrete serotonin

115
Q

What is a GIST?

A

Gastrointestinal stromal tumor originating from interstitial cells of Cajal

c-KIT positive and often requires surgical resection

116
Q

What is MALToma?

A

Marginal zone B-cell lymphoma associated with H. pylori infection

Can enter remission with eradication of H. pylori

117
Q

What is MALToma associated with?

A

H. pylori

MALTomas are marginal zone B-cell lymphomas that can go into remission if H. pylori is eradicated.

118
Q

What are the two types of causes for MALToma?

A
  • Translocation
  • Antigen stimulation alone (H. pylori)

both increase NF-kb

Translocation do not respond to H. pylori eradication due to genetic issues.

119
Q

What can MALToma turn into?

A

Aggressive diffuse large B-cell lymphoma

120
Q

What can Aspirin or NSAIDs induce?

A

Acute gastritis or reactive gastropathy

121
Q

What does AMAG cause in relation to Vitamin B12?

A

Autoantibodies to:
1. Proton Pump (H+/K+ ATPase)
2. Intrinsic Factor

Reduced Pepsinogen d/t Chief Cell destruction

This leads to pernicious anemia if Vitamin B12 is not absorbed.

122
Q

Define dysphagia

A

Difficulty or discomfort swallowing

123
Q

What is odynophagia?

A

Pain while swallowing

124
Q

What are symptoms of esophageal obstruction?

A
  • Dysphagia
  • Odynophagia

Symptoms typically progress from solids to liquids.

125
Q

What is peristalsis?

A

Rhythmic contraction of muscles

126
Q

What is Zenker Diverticulum?

A

Impaired relaxation & spasm of cricopharyngeal muscle after swallowing
Pharyngoesophageal Diverticulum (Zenker)

Zenker Diverticulum more common than Epinephric Diverticulum

127
Q

What are the two types of esophageal tears?

A
  • Mallory-Weiss Syndrome
  • Boerhaave Syndrome
128
Q

What is the most common congenital malformation of the esophagus?

A

Esophageal atresia & Tracheoesophageal fistula

129
Q

What is the likely diagnosis for a massively dilated esophagus on an X-ray?

A

Achalasia

130
Q

What causes achalasia?

A

Failure of the LES to relax after swallowing

131
Q

What is the primary form of achalasia?

A

Idiopathic

132
Q

What are two types of esophageal dysmotility syndromes aside from achalasia?

A
  1. Nutcracker Esophagus
  2. Diffuse/Distal Esophageal Spasm (DES)
133
Q

What is an esophageal web?

A

Semi-circumferential protrusion of a thin mucosa fold
usually in upper esophagus

c/c with Schatzki Ring - circumferential & thick

134
Q

What is a Schatzki ring?

A

Circumferential and thick structure in the distal esophagus
Relatively common
steakhouse syndrome

135
Q

What organisms might be encountered in an immunocompromised patient with infectious esophagitis?

A
  • Herpes
  • CMV
  • Fungus (Candida)
136
Q

What causes GERD?

A

Reflux of gastric acid or contents back into the esophagus

137
Q

What are common symptoms of GERD?

A

Heartburn

138
Q

What is Barrett esophagus?

A

Metaplasia in the lower esophagus from squamous to intestinal type mucosa

139
Q

What is required to make a histologic diagnosis of Barrett esophagus?

A

Presence of goblet cells and dysplasia

140
Q

What does the presence of dysplasia in Barrett esophagus imply?

A

Increased risk of invasive esophageal adenocarcinoma

141
Q

What are typical symptoms of esophageal cancer?

A
  • Progressive dysphagia
  • Odynophagia
  • Weight loss
142
Q

What are the risk factors for adenocarcinoma of the esophagus?

A
  • Alcohol
  • GERD
  • Male
  • Caucasian
  • Obesity
143
Q

What is the precursor lesion for adenocarcinoma?

A

Intestinal metaplastic mucosa of Barrett esophagus

144
Q

What causes gastroesophageal varices?

A

Portal hypertension

145
Q

What is thought to cause eosinophilic esophagitis?

A

Food allergy

146
Q

Define ileus

A

Mechanical occlusion or functional paralysis of the bowel

147
Q

What are signs and symptoms of ileus?

A
  • Nausea
  • Vomiting
  • Abdominal pain
  • Distention
  • Obstipation (severe constipation)
148
Q

What are the four most common causes of mechanical intestinal obstructions?

A
  • Incarcerated hernia
  • Adhesions
  • Volvulus
  • Intussusception
149
Q

What is Ogilvie syndrome?

A

Intestinal pseudo-obstruction
defined as dilatation of the colon - usually the cecum & ascending colon

associated with post-operative state and critically ill hospitalized patients

150
Q

What are common causes of intestinal perforation?

A
  • Foreign bodies
  • Ulcers
  • Diverticulitis
  • Trauma
151
Q

What is hematochezia?

A

Passage of bright red blood in stool

152
Q

What is melena?

A

Passage of dark, tarry stools

153
Q

What are watershed zones?

A

Zones where blood supply switches, making them vulnerable to ischemia

154
Q

What are the three major clinical GI tract ischemic syndromes?

A
  • Ischemic colitis
  • Acute mesenteric ischemia
  • Chronic mesenteric ischemia
155
Q

What is the typical symptom for chronic mesenteric ischemia?

A

Postprandial pain

156
Q

What is prandial pain?

A

Pain after eating, usually leads to food fear due to pain associated with eating.

Prandial pain is often due to chronic mesenteric ischemia.

157
Q

What is the common cause of prandial pain?

A
  • Chronic mesenteric ischemia
  • Stenosis of mesenteric vessels - can be fixed with revascularization repair

Revascularization repair addresses the underlying issue causing the ischemia.

158
Q

What are typical symptoms of chronic mesenteric ischemia?

A
  • abdominal postprandial pain (30-60 mins after eating)
  • “food fear”

weight loss, constipation or diarrhea

159
Q

What is a common complication of therapeutic radiation therapy?

A

Radiation enterocolitis, which can be acute or chronic.

Acute radiation enterocolitis may present with necrosis, anorexia, cramps, and fever, while chronic can lead to radiation proctitis.

160
Q

What is angiodysplasia?

A
  • Tortuous dilations of mucosal and submucosal capillaries, venules & veins
  • Primarily occurring in older adults

It typically presents in the cecum/right colon and accounts for 20% of major lower GI bleeds.

161
Q

What are the classic symptoms of hemorrhoids?

A

Rectal pain, itching, bleeding, and prolapse.

Complications can include thrombosis, bleeding, ulceration, fissures, and prolapse.

162
Q

What are the four categories of diarrhea?

A
  • Secretory diarrhea - persist w/ fasting
  • Osmotic diarrhea - abates w/ fasting
  • Malabsorptive diarrhea - relieved w/ fasting
  • Exudative diarrhea - persist w/ fasting
163
Q

What causes malabsorptive diarrhea?

A

Failure of nutrient absorption, often relieved by fasting.

Steatorrhea is a common symptom associated with malabsorptive diarrhea.

164
Q

What are the phases of nutrient absorption affected by malabsorption?

A
  • Intraluminal digestion - Gut lumen
  • Terminal digestion - brush border SI lumen
  • Transepithelial transport - SI epithelium
  • Lymphatic transport of absorbed lipids

Disturbances in any of these phases can lead to malabsorption.

165
Q

What are common lab tests for malabsorption?

A
  • Fecal fat for steatorrhea
  • Pancreatic insufficiency screen
  • CBC for anemia
  • PT/INR for vitamin K deficiency
  • CMP for albumin levels and increased alkaline phosphatase

These tests help identify the underlying causes of malabsorption.

166
Q

What is the pathogenesis of celiac disease?

A

Immune-mediated injury to small intestinal mucosa exposed to wheat gliadin due to HLA-DQ2 or DQ8 susceptibility.

The alpha-Gliadin peptide triggers an immune response leading to inflammation and damage.

167
Q

What are the clinical features of celiac disease?

A
  • Malabsorptive diarrhea
  • Weight loss
  • Fatigue
  • Dermatitis herpetiformis

Symptoms may improve with a gluten-free diet.

168
Q

What causes abetalipoproteinemia?

A

Inability to transfer lipids to nascent apolipoprotein B, leading to lipid accumulation inside enterocytes.

Infants with this condition may present with failure to thrive, diarrhea, and steatorrhea.

169
Q

What is the cause and clinical findings of Whipple disease?

A
  • Caused by Tropheryma whipplei
  • Malabsorptive diarrhea d/t impaired lymph drainage

Symptoms can include abdominal pain and potential neurologic manifestations.

170
Q

What are the symptoms of cholera?

A

Secretory watery diarrhea, often described as ‘rice water stools,’ leading to dehydration.

Cholera is caused by human fecal contamination of drinking water.

171
Q

What is the treatment for Pseudomembranous Colitis?

A

Oral vancomycin or metronidazole; fecal microbial transplantation may also be considered.

Diagnosis involves detecting toxigenic C. difficile and correlating with clinical symptoms.

172
Q

What is the common cause of viral gastroenteritis in children?

A

Rotavirus, which is most common in kids under 2 years of age.

A vaccine is available to prevent severe cases in this population.

173
Q

What is the typical presentation of small bowel bacterial overgrowth syndrome?

A

Watery diarrhea and/or steatorrhea with anemia due to B12 deficiency.

Imparied intestinal motility - causing bacterial overgrowth in the small bowel (small intestine)

174
Q

What are the criteria for diagnosing IBS?

A

Rome Criteria for Dx:
Recurrent abdominal pain - at least 1 day/week for the last 3 months + altered bowel habits ( with 2 or more of the following:
* pain related to defecation
* changes in frequency of stool (diarrhea or constipation)
* changes in form/appearance of stool

175
Q

What is the prevalence of IBS?

A

1 in 10

176
Q

Does IBS increase cancer risk?

A

No increased cancer risk

177
Q

What dietary approach may benefit IBS patients?

A

Low FODMAP diet

178
Q

What are alarm signs for IBS?

A
  • Older onset
  • GI bleeding
  • Nocturnal diarrhea
  • Progressive abdominal pain
  • Unexplained weight loss
  • Increased fecal calprotectin/lactoferrin
  • Family history
179
Q

What is the general idea behind Inflammatory Bowel Disease (IBD)?

A

Chronic diseases due to altered mucosal immune interaction leading to intestinal and extraintestinal manifestations.

180
Q

What are the two main types of IBD?

A
  • Ulcerative colitis
  • Crohn’s disease
181
Q

What are common symptoms of IBD?

A
  • Diarrhea
  • Abdominal pain
  • Variable blood in stool
182
Q

What are extraintestinal manifestations associated with IBD?

A
  • Enteritis associated arthritis
  • Asthma
  • Pyoderma gangrenosum
  • Erythema nodosum
  • Uveitis/iritis
  • Primary Sclerosing Cholangitis
183
Q

What is the pathogenesis of IBD?

A

Genetic and environmental inputs result in altered host immune response to gut microbiome.

184
Q

What are the three general ideas regarding the pathogenesis of IBD?

A
  • Hygiene hypothesis
  • Bacterial antigens activate innate/adaptive immune response
  • Genetic/cytokine prompted increase in permeability of tight junctions
185
Q

What are skip lesions in Crohn’s disease?

A

Separate, delineated areas of involvement with normal areas.

186
Q

What areas of the bowel are most commonly involved in Crohn’s disease?

A

Usually terminal ileum, ileocecal valve, and cecum, but can occur anywhere in the GI tract.

187
Q

What are major diagnostic microscopic features of Crohn’s disease?

A
  • Transmural inflammation
  • Fissures
  • Ulcers
  • Crypt abscesses
  • Non-caseating granulomas
188
Q

What are the clinical presentations of Crohn’s disease?

A
  • Intermittent episodes of diarrhea
  • Abdominal pain
  • Blood or mucus in stool
  • Sometimes fever
189
Q

What are the complications of Crohn’s disease?

A
  • Perianal/rectal fistula/abscess
  • Intestinal obstruction
  • Pericolic/retroperitoneal abscess
  • Intestinal perforation
  • Iron deficiency anemia
  • Risk of colon cancer
190
Q

What is the first-line treatment for Ulcerative Colitis?

A

5-ASA

191
Q

What is the most common type of polyp?

A

Adenomatous and hyperplastic colon polyps

192
Q

What is the hallmark of an adenomatous polyp?

A

Epithelial dysplasia without lamina propria or submucosal invasion.

193
Q

At what age should screening colonoscopy begin?

A

At 45 unless there are red flags or 10 years before the age at which a first-degree relative was diagnosed with colon cancer.

194
Q

What is the molecular defect in Peutz-Jeghers syndrome?

A

Molecular defect in tumor suppressor gene STK11.

195
Q

What is the most common presentation of Peutz-Jeghers syndrome?

A

Bowel obstruction due to intussusception in older children.

196
Q

What is the risk of colorectal cancer in patients with Familial Adenomatous Polyposis (FAP)?

A

Nearly 100% by age 40.

197
Q

What is the most common syndromic form of colorectal cancer?

A

HNPCC/Lynch syndrome

198
Q

What is the typical location of cancers associated with HNPCC?

A

Cecum (right colon in general).

199
Q

What is the cardinal rule for older patients presenting with iron deficiency anemia?

A

Need to work them up for colon cancer; endoscopy with biopsy is crucial.

200
Q

What are the common causes of peritonitis?

A
  • Necrosis/perforation of the intestinal viscera
  • Chemical causes (free blood, gastric/pancreatic juices)
201
Q

What are the clinical implications of right vs left sided colon cancer in terms of presenting symptoms?

A

Right colon cancer presents with anemia from occult blood loss. Left colon cancer presents with obstructive symptoms.

202
Q

What is the cardinal rule for older patients presenting with iron deficiency anemia?

A

Work them up for colon cancer; endoscopy with biopsy is crucial.

203
Q

What is our best predictor of prognosis in colorectal cancer (CRC)?

A

TNM Stage, determined by depth of invasion, lymph node status, and +/- distant metastases.

204
Q

What is the most common site of distant metastasis for colorectal cancer (CRC)?

A

Liver

205
Q

What is the best use of CEA in CRC?

A

To determine treatment response and recurrence of CRC.

206
Q

What is the most common type of cancer of the anal canal?

A

Squamous Cell Carcinoma

207
Q

What causes Squamous Cell Carcinoma of the anal canal?

A

HPV

208
Q

What is the pathogenesis of acute appendicitis?

A

Obstruction by fecalith, tumor, or worms leading to bacterial overgrowth and inflammation.

209
Q

What are the clinical signs and symptoms of acute appendicitis?

A

Acute abdomen, guarding, rebound tenderness.

210
Q

What lab findings are associated with acute appendicitis?

A

Increased CRP, neutrophilia.

211
Q

What is a key physical exam finding for acute appendicitis?

A

Deep tenderness at McBurney’s point (⅓ from ASIS).

212
Q

What is a potential complication of acute appendicitis?

A

Perforation.

213
Q

What is the connection between mucinous tumors of the appendix and pseudomyxoma peritonei?

A

Mucinous tumors can lead to pseudomyxoma peritonei, which is mucinous ascites caused by low grade mucinous neoplasms or ruptured adenocarcinoma.

214
Q

What is the most common tumor of the appendix?

A

Carcinoid tumors

215
Q

Are carcinoid tumors of the appendix benign or malignant?

A

Considered low grade malignancies.

216
Q

What factors determine the prognosis for carcinoid tumors in the GI tract?

A

Localization (originating site) and biology (size/mitotic rate).

217
Q

What is carcinoid syndrome?

A

Secretion of serotonin due to massive metastatic load in the liver bypassing liver MAO inactivation to 5-HIAA.

218
Q

When is carcinoid syndrome seen?

A

With liver metastases.

219
Q

What is a major complication of carcinoid syndrome?

A

Right heart issues.

220
Q

What lab test might assist in the diagnosis of carcinoid syndrome?

A

High plasma Chromogranin A.

Pathology Winter Exam 2 (4 decks)

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