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MHD 2- Exam 1 > Lecture Review > Flashcards

Lecture Review Flashcards

1
Q

What parasite is this image associated with?

A

Babesia

(presence of tetrad)

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2
Q

What specific parasite is this associated with?

A

Plasmodium Falciparum

(Banana gametocyte)

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3
Q

ID the parasite this image is associated with

A

Acid fast of Cryptosporidium oocysts

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4
Q

ID the parasite this image is associated with

A

Fluoresence of Cryptosporidium Oocysts

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5
Q

What parasite is this?

A

Giardia

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6
Q

What organism is this associated with?

A

This is a cyst for Giardia

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7
Q
A

Trichomonas Vaginalis

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8
Q

What is this and what is it associated with?

A

Amastigote

Intracellular form of Leishmania/Trypanosomiasis found in human

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9
Q

This is the result of what?

A

Cutaneous Leishmaniasis

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10
Q

What is this from?

A

DFA (fluoresence) of Pneumocystis Jiroveci (Carinii)

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11
Q

What is this?

A

Silver Stain of Pneumocystis Jiroveci (Carinii). Shows empty cysts which have expelled the protozoa.

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12
Q

Interpret this Serology:

HBsAg: negative

anti-HBc: negative

anti-HBs: negative

A

Susceptible

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13
Q

Interpret this Serology:

HBsAg: negative

anti-HBc: positive

anti-HBs: positive

A

Immune due to natural infection

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14
Q

Interpret this Serology:

HBsAg: negative

anti-HBc: negative

anti-HBs: positive

A

Immune due to hepatitis B vaccination

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15
Q

Interpret this Serology:

HBsAg: positive

anti-HBc: positve

IgM anti-HBc: positive

anti-HBs: negative

A

Acutely infected

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16
Q

Interpret this Serology:

HBsAg: positive

anti-HBc: positve

IgM anti-HBc: negative

anti-HBs: negative

A

Chronically infected

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17
Q

Interpret this Serology:

HBsAg: negative

anti-HBc: positve

anti-HBs: negative

A

Interpretation unclear! (4 possibilities)

  1. Resolved infection (most common)
  2. False positive anti-HBc (thus susceptible)
  3. “Low level” chronic infection
  4. Resolving acute infection
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18
Q

What liver disease is this associated with?

(hint: these are plasma cells)

What else might you see?

A

Autoimmune hepatitis

This image shows plasma cells creeping into the lobule. You would also expect to see interface hepatitis.

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19
Q

Positive blue staining for iron in liver as in the image, is indicative of what disease process?

A

Hemochromatosis

A disease of iron overload

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20
Q

What is the phenomenom in the bottom left photo called and what is it associated with?

A

“Scalloped edges”

Celiac Disease

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21
Q

What is pyloric stenosis and what are its symptoms (3)?

A

Congenital hypertrophy of the smooth muscle of the pylorus

Sx: projectile vomiting in first 2-6 weeks of life, visible peristalsis, olive-like mass in abdomen.

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22
Q

What is the most likely cause for acute gastritis? chronic?

A

acute: impairment of protective system (via NSAIDs, direct injury, ingestion, etc.)

chronic: H. Pylori

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23
Q

What stains are useful for highlighting H. pylori (2)?

A
  • methylene blue stain
  • Warthrin-starry stain
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24
Q

Describe the pathogenesis of Autoimmune chronic gastritis and what occurs as a result.

Is the risk of adenocarcinoma affected?

A
  • There are antibodies to parietal cells and IF
  • Antrum is spared
  • Results in B12 deficiency (IF loss) and resulting anemia
  • Also decreased pepsinogen (acid) levels (chief cells loss)
  • Increased risk of gastric adenocarcinoma
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25
Q

What are the symptoms and acute PUD?

Chronic?

Describe the ulcers in each case.

A

Acute:

  • N/V w/ coffee-ground hematemesis
  • Ulcers: <1cm and sharply demarcated

Chronic:

  • Epigastric burning or aching that is worse at night
  • Relieved w/ akali or food
  • Nausea, bloating, belching
  • Could be caused by ZE
  • Ulcers: Usually solitary and sharply punched out
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26
Q

What is the relationship between location and prognosis for a carcinoid tumor?

What kind of tissue do these tumors arise from?

A

These tumors arise from neuroendocrine organs (G-cells of stomach)

Location determines prognosis:

  1. Foregut is resectable
  2. Midgut is most aggresive
  3. Can also be located in the hindgut
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27
Q

Gastrointestinal Stromal Tumor (GIST)

Pathogenesis?

What does it look like?

Treatment?

A
  • Mesenchymal neoplasm of interstitial cells of cajal
  • 75-80% w/ GOF mutation in gene encoding tyrosine kinase c-KIT
  • Solitary, well circumscribed, fleshy, submucosal mass
  • Tx: Surgical resection (if possible); Imatinib (there is often resistance)
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28
Q

What are the (3) general causes for Gastric Adenocarcinoma?

A
  1. H. Pylori
  2. EBV
  3. Mutation
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29
Q

Describe the (2) types of mutation which can lead to Gastric Adenocarcinoma.

What are the mutations?

What type of adenocarcinoma do they cause?

What are the differences in the tumor types and sexes affected?

Other key points w/ treatment and clinical findings?

A

Diffuse Type

  • Caused by mutation of CHD1 causing E-cadherin fxn loss
  • Infiltrative growth and discohesive cells w/ large mucin vacuoles (signet ring cells)
  • Equal incidence between men and women
  • Linitis plastica (thick stomach wall)

Intestinal type

  • Familial APC mutations
  • Bulky, glandular, exophytic mass or ulcerated tumor
  • Men twice as common
  • Tx: Surgical resection (chemo is not effective)
    *
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30
Q

Intestinal type M__etastatic Gastric Adenocarcinoma is called what and is located where?

Diffuse type?

A

Intestinal: Sistery Mary Joseph nodule- Mets to Periumbilical region

Diffues: Krukenberg tumor- Mets to Bilateral ovaries

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31
Q

What type of muscle makes up the upper 2/3rds of the esophagus? lower 1/3rd?

A

Striated = upper

smooth= lower

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32
Q

What is achlasia and what is one of the key secondary etiologies?

Pathogenesis?

How does it look on barium swallow?

A
  • Incomplete relaxation of LES and disordered motility of the esophagus (anti-peristalsis); Esophageal dilatation
  • Pathogenesis: destruction of myenteric plexus
  • Birds beak deformity on barium swallow

Associated w/ Chagas disease

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33
Q

Boerhaave syndrome

What is it and what is a key finding associated?

A

Transmural esophageal rupture from severe vomiting

Very high morbidity/mortality, so always a medical emergency

Associated with Subcutaneous emphysema of skin (rice krispy feeling when you press on patient’s skin)

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34
Q

What are the (3) M’s of Herpes Simplex virus associated with one of the forms of esophagitis?

A

Multinucleation, Molding and Margination

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35
Q

All forms of Esophagitis show what (3) histologic changes?

A
  1. Basal layer hyperplasia (>20% of mucosal thickness)
  2. Lamina Propria papillae which reach top 1/3rd of mucosa
  3. Intra-epithelial eosinophils
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36
Q

Name the corresponding LNs that SCC in each of the following parts of the esophagus spreads to:

Upper 1/3rd

Middle 1/3rd

Lower 1/3rd

A

Upper: Cervical LNs

Middle: Mediastinal/ tracheobronchial LNs

Lower: Celiac/gastric LNs

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37
Q

Name the Vibrio Cholerae exotoxin responsible for causing disease.

A

AB Type ADP-ribosylating toxin

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38
Q

What level of inoculum is needed for a campylobacter infection?

A

Low! As low as 500 organisms

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39
Q

Clinical manifestation of Campylobacter Jejuni

What disease is it affliated with?

A

Fever (1 day) followed by sever abdominal pain and diarrhea w/ blood, pus and campy in feces

Associated w/ Guillain-Barre Syndrome (ascending paralysis)

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40
Q

What are the roles of Bab A, Vac A and Cag A, in h.pylori infection?

A

Bab A: Used for adherence. Binds to lewis blood group antigens

Vac A: Vacualiting cytotoxin that inserts into epithelial cell membranes forming nutrient releasing poor. Also inserts into mitochondria to release cytochrome C and induce apoptosis.

Cag A: Functions to promote cytokine production

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41
Q

Volvulus

Where does it tend to happen for children? adults?

A

Twisting of the bowel around its mesentery. Leads to obstruction and infarction.

Tends to be midgut for children and sigmoid for adults.

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42
Q

Meckel’s diverticulum

A

Persistence of the omphalomesenteric duct.

Known as the disease of “2’s”

(2% of pop.; 2x likely for men; 2 main complications- pain w/ inflammation and hemorrhage w/ ulcer)

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43
Q

Hirschsprung Disease

A

Form of megacolon in which the absence of ganglion cells (enteric neurons) leads to premature death of neural crest cells migrating from cecum to rectum. Mostly in males.

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44
Q

What effect does pancreatic insufficiency have on neutral fat? D-xylose absorption test?

A
  • Increased neutral fat
  • Normal D-xylose absorption test (urinary excretion)
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45
Q

Abetalipoproteinemia

A

Decreased synthesis of apo B which results in decreased ability to generate chylomicrons.

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46
Q

What is the skin issue associated with Celiac disease? How do we diagnose this disease (be specific)?

A
  • Dermatitis herpetimormis (skin blistering disease)
  • Diagnosis via:
  1. Biopsy: Villous atrophy w/ inc. intraepithelial lymphocytes (CD8)
  2. Serotype: anti-TTG, anti-deaminated gliadin, anti-endomysial antibodies (If pts are IgA deficienct, IgG tests are needed)
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47
Q

Both collagenous and lymphocytic colitis cause what clinical presentation?

A

Chronic watery diarrhea (3-20 non-bloody stools per day)

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48
Q

What is the pathogenesis and clinical presentation in whipple disease?

A

Pathogenesis: Tropheryma whippleli bug is engulfed by macrophages

Sx: Malabsorption, lymphadenopathy (due to congestion of lymph vessels w/ macrophages), and arthritis

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49
Q

What are the key differences between Crohn’s Disease and Ulcerative Colitis, in terms of…

Pt. Demographic? Location? Gross mrophology? Microscopic changes? Complications? Intestinal Manifestation? Key Extraintestinal manifestations?

A

Crohn’s: White Jewish folks, with non-bloody diarrhea, cobblestoning, skip lesions throughout GI tract, and strictures

UC: Wealthy western folks, with bloody diarrhea, pseudopolyps limited to the colon, and megacolon

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50
Q

Juvenile polyps and malignancy

A

Mostly occur sporadically in rectum of children < 5y/o

If single, no malignant potential.

If multiple, increased risk of adenocarcinoma.

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51
Q

Hamatomatous (Peutz-Jeghers syndrome)

Pathophysiology? Presentation? Malignant potential?

A
  • Multiple non-malignant hamartomas throughout the GI tract
  • Sx: Hyperpigmented melanotic macules of mouth, lips, genatalia and hands
  • Increased CRC risk (although the polyps themselves have NO malignant potential)
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52
Q

What are adenomatous polyps and what are they precursors to? What are the different types (2) and which is more likely to be dangerous?

A

These are benign polyps that are precursors to the majority of colorectal adenocarcinomas.

There are peduculated types and sessile types. Sessile is more likely to grow to cancer.

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53
Q

Where do sessile serrated adenoma occur? What is the main mechanism for their pathogenesis?

A

Right colon

DNA mismatch repair

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54
Q

Familial Adenomatous Polyposis

What is it and what does it lead to? What causes it?

A

It is a condition in which patients develop 100-1000 polyps, due to an autosomal dominant defect in the APC gene (Ch5q21)

100% development into colorectal adenocarcinoma

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55
Q

What are the (2) variants of FAP? Describe them.

A

Gardner syndrome- same as FAP + osteomas (mandible, skull, and longbones), epidermal cysts, desmoid and thyroid tumors, and dental abnormalities

Turcots syndrome- Intestinal adenomas + tumors of CNS which depend on the the type of mutation (APC: medulloblastoma/ repair mutation: glioblastoma)

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56
Q

Hereditary nonpolyposis colorectal cancer (Lynch syndrome)

What is it and what causes it?

A

Associated w/ FAP but fewer number of polyps. Cancer occurs at a younger age than sporodic cancers.

Caused by mutation in DNA mismatch repair genes

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57
Q

What are the (2) main molecular pathways to CRC and what specific conditions are they each associated with?

A
  1. APC/WNT pathway: APC is a neg. regulator of Beta-Catenin. Double knockout of APC increases B-catenin, which translocates to the nucleus and activates transcription of MYC, Cyclin D1, etc. Associated w/ FAP and sporodic colon cancer.
  2. DNA Mismatch Repair: spelling error in coding region. Affect on MLH, MSH, and PMS genes. Associated w/ HNPCC
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58
Q

Right sided vs Left sided CRC

A

Right: asymptomatic for longer because colon diameter is larger. First symptom for right side is anemia due to blood loss/ulceration

Left: smaller diameter so obstruction occurs much quicker (changes in BM habits). Tend to see napkin ring lesion.

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59
Q

What cancer type is most commonly found in the rectum? The anus?

A

Rectum: adenocarcinoma

Anus: SCC

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60
Q

Name/describe the (3) Neoplasm types associated w/ the appendix

A
  1. Mucocele: benign dilatation o lumen by mucinous secretion
  2. Mucinous cystadenoma: proliferation of benign neoplastic cells and dilation which may rupture
  3. Mucinous cystadenocarcinoma- invasion of neoplastic cells
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61
Q

Pseudomyxoma peritonei

A

Distention of peritoneal cavity by the presence of semisolid mucin and epithelial mucin producing implants and/or malignant cells. Possible complication of mucinous tumor of the appendix.

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62
Q

What separates the upper GI system from the lower GI system?

A

Ligament of Triez

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63
Q

Hematochezia

A

Bright Red Blood Per Rectum (BRBPR)

Usually denotes LGI bleed but could also be UGI bleed

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64
Q

What are the top (4) differentials for an UGI bleed?

A
  1. PUD
  2. Esophageal varices
  3. Erosive esophagitis
  4. Mallory-Weiss tears
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65
Q

Nasogastric Aspiration

What counts as a (+) result? What counts as a (-) result? WHat result types are indeterminant?

A

(+): blood, +/- bile

(-): bile, no blood

Indeterminate (fake negative): no blood and no bile

EGD usually ends up being done anyway.

66
Q

When dealing w/ a UGI bleed, what is the usefullness of a pre-endoscopic IV PPI? post-endoscopic IV PPI?

A

Pre-endoscopic IV PPI: No impact on rebleeding, mortality, or need for surgery. Does accelerate resolution of bleeding and decreased need for endoscopic therapy.

Post-endoscopic IV PPI: Very effective for decreasing likelihood of rebleeding, need for surgery and mortality

67
Q

What are the top (4) differentials for LGI bleeding?

A
  1. Diverticulosis
  2. Colitis (Ischemic, IBD, Radiation)
  3. Hemorrhoids
  4. Postpolypectomy
68
Q

What are the (3) different ways to define diarrhea?

A
  1. High stool frequency (>3/day)
  2. High quantity of stool (>200g of stool/day)
  3. Abnormally loose stool
69
Q

What are the special populations to keep an eye out on if they hve diarrhea?

A
  1. Elderly
  2. Immunocompromised
  3. IBD pts
  4. Pregnant pts
70
Q

How common are infectious causes of chronic diarrhea?

A

Uncommon for immunocompetent people. Consider giardia if patient is exposed to young children or in contact w/ lakes/streams

71
Q

What are the (5) classifications for chronic diarrhea?

A
  1. Secretory
  2. Osmotic
  3. Steatorrhea
  4. Impaired Mobility (less important)
  5. Inflammatory
72
Q

What is the most common cause for Steatorrhea?

A

Small intestine bacterial overgrowth!

(Can also occur due to celiac, whipples, etc.)

73
Q

What are the (5) ways to define constipation?

A
  1. Straining during defecation
  2. Passage of lumpy or hard stool
  3. Sensation of incomplete defecation
  4. Use of manual maneuvers to facilitate BM
  5. Freq. of less than (3) BMs per week
74
Q

What are the general alarm signs associated with constipation? (5)

A
  1. Age > 50
  2. New onset in the elderly
  3. Weight loss
  4. History of cancer (personal and family) or radiation or resection
  5. Palpable mass on ecam
75
Q

What are the criteria to qualify for IBS?

A
  1. Recurrent abdominal pain 3x/mo
  2. 2 or more of the following:
    • Improvement with defecation
    • Change in freq. of stool
    • Change in appearance of stool

(No further testing unless alarm symptoms present)

76
Q

What is the stool pattern for IBS? How does this impact treatment?

A

Could be either constipation or diarrhea. Treatment is based on the stool pattern.

Constipation- psyllium/miralax

Diarrhea- loperamide

77
Q

80% of acute pancreatitis cases are associated with… (2 things)

A

Biliary tract disease of alcoholism

78
Q

What is the clinical presentation for acute pancreatitis? (6)

A
  1. Abdominal pain
  2. Elevated plasma amylase/lipase
  3. Hypocalcemia
  4. ARDS
  5. DIC
  6. Fluid sequestration
79
Q

Predisposing factors for chronic pancreatitis?

A
  1. Longterm alcohol abuse
  2. Long standing obstruction
  3. CF
  4. Idiopathic
80
Q

5 key symptoms/presentations associated with Chronic Pancreatitis

A
  1. Recurrent attacks of abdominal pain
  2. Recurrent attacks of jaundice or vague indigestion
  3. Exocrine pancreatic insufficiency (Steatorrhea)
  4. Endocrine pancreatic insufficiency (DM)
  5. Pancreatic calcifications of imaging
81
Q

What is the precursor lesion for Pancreatic Carcinoma (aka infiltrating ductal adenocarcinoma of the pancreas)

A

Pancreatic Intraepithelial Neoplasia (PanIN)

(caused by mutations in K-RAS, p16 and p53)

82
Q

Most common location for pancreatic carcinoma (head, body, tail, or diffuse?)

What basic symptom often separates the (3) types?

A

Head of the pancreas is most common

Leads to obstructive jaundice (unlike the others which tend to be clinically silent)

83
Q

Desmoplastic response

A

Proliferation of dense stromal fibrosis in response to a pancreatic tumor

84
Q

What is one of the most common symptoms associated w/ pancreatic carcinoma, and why?

A

Pain because it often invades into adjacent nerves

85
Q

Key tumor markers for pancreatic carcinoma

A

Elevated CA19-9 and CEA

86
Q

Trousseau Sign

A

Migratory thrombophlebitis

(Spontaneously appearing and disappearing venous thromboses which occur in 10% of Pts with pancreatic carcinoma.)

87
Q

Key points about serous cystadenoma

(Behavior, gross morphology, histopath, key clinical points)

A

Benign, small cysts, cuboidal cells, non-specific symptoms

88
Q

Key points about Mucinous Cystic Neoplasms

(Behavior, gross morphology, histopath, key clinical points)

A

Almost exclusively women, could be benign or malignant, not connected to main pancreatic duct, lined by columnar cells, Body/Tail pancreas

89
Q

Key points about Intraductal papillary mucinous neoplasms (IPMN)

(Behavior, gross morphology, histopath, key clinical points)

A

Benign to malignant, arise in main pancreatic duct/major branch, lined by columnar cells, Men > women, Head of Pancreas

90
Q

The Sand fly serves as a vector for what? Tsetse fly? Triatomid bug?

A

Sand fly- Leishmania

Tsetse fly- African trypanosomiasis (T. brucei gambiense and rhodesiense)

Triatomid bug- American trypanosomiasis (T. Cruzi)

91
Q

What kind of bilirubin is detected in bilirubinuria? What are the causes (common and rare)?

A

Conjugated bilirubin (unconjugated is water insoluble).

Hepatocellular disease is the most common causes, but Dubin-Johnson and Rotor Syndrome can also cause it (due to inability of hepatocytes to secrete conjugated bilirubin into the bile).

92
Q

What is the etiology of primary Biliary Cirrhosis? What tests would we run and what would we expect?

A

It is autoimmune

+ antimitochondrial antibody, inc. alkaline phosphatase, and inc. total bilirubin (advanced disease)

93
Q

What is the key histological finding for Primary Biliary Cirrhosis? Describe it.

A

Florrid duct lesion

Periductal inflammation w/ granuloma formation and duct destruction. Indicitive of lymphocyte infiltrate.

94
Q

What is Primary Sclerosing Cholangitis and what disease is it associated with? What does it progress to?

A

Onion skinned pattern of obliterative fibrosis of intrahepatic and extrahepatic bile ducts w/ inflammation and dilation of preserved segments (beading).

Progreses to end stage liver disease.

95
Q

GIlbert’s Syndrome

A

Isolated elevation of total and direct bilirubin after physical activity in particular, due to genetic defect in UGT (so can’t conjugate).

Mostly in men. No follow-up needed.

96
Q

Courvoiser sign

A

States that in the presence of an enlarged gallbladder which is nontender and accompanied with mild jaundice, the cause is unlikely to be gallstones.

97
Q

What signs/ tests make you think a patients hyperbilirubinemia is intrahepatic? Extrahepatic?

A

Hepatocellular:

  • Transaminases elevated > 700
  • Dec. serum albumin
  • Alkaline phospatase only 1.5-2x normal
  • Thrombocytopenia

Obstructive:

  • Transaminases (
  • Alkaline phosphatase 5-10x normal
98
Q

What key molecules are absorbed in the duodenum? In the Ileum?

A

Duodenum: Calcium and Iron

Ileum: Vitamin B12 and Bile salts

Everything else is the jejunum (90% of absorption)

99
Q

Colonic Salvage

A

Bacteria act on carb/fiber to produce short-chain fatty acids and the colon can absorb up to 500 kcal/d as SCFAs/lactate. This is particularly useful in short gut syndrome.

100
Q

What are the (2) Helminths that have the ability to multiply w/in the human host?

A
  1. Strongyloides
  2. Hymenolepsis nana (dwarf tapeworm)

Can autoinfect and are therefore chronic

101
Q

List the (3) clinical phases of trichinosis spiralis

A

Phase I:

  • 24-72 hours
  • Diarrhea, N/V, and abdominal pain

Phase II:

  • 2-3 weeks
  • Fever, myalgia, periorbital edema
  • CNS/cardiac (major cause of death)

Phase III: Recovery

102
Q

Clinical presentation of strongyloides stercoralis. Who does it effect?

A
  • Severe diarrhea
  • Pneumonia
  • Eosinophilia
  • Septicemia

Effects the immunocompromised

103
Q

What nematodes have microfilariae which circulate in the bloodstream? (2)

A
  1. Wuchereria Bancrofti (Lymphatic Filariasis)
  2. Loa loa
104
Q

What is the optimal method for diagnosis for Onchocerciasis (river blindness)?

A

Skin snips

105
Q

What are the (4) tapeowrms w/ adult stages w/in the human intestine? What foods are they associated w/?

A
  1. Taenia saginata (Beef)
  2. Taenia solium (Pork)
  3. Diphyllobothrium latum (Fish)
  4. Hymenolepsis nana (n/a)
106
Q

How are the shistome species acquired? Where do they develop into adults? Where do they lay eggs?

A

Schistosome species are acquired from skin exposed to infested water. They develop into adults while in the liver, and then mate. Ova are then produced in the large intestine and passed into the stool.

107
Q

What organism is critical for the schistosoma life cycle?

A

The snail!

108
Q

Mechanism for human acquisition of infection by Opisthorchis species? Paragonimus westermani? What is another name for each of these species?

A

Opisthorchis (liver fluke)- Undercooked fish w/ cysts

Paragonimus (lung fluke)- Crayfish/crab

109
Q

What is the pathogenesis of swimmer’s itch?

A

Also known as cercarial dermatitis.

Accidental infection of human swimmers w/ duck schistosome, which can’t penetrate beyond the skin.

110
Q

Wucheria Bancrofti symptoms/presentation (4)

A
  1. Cough from microfilariae in lungs
  2. Lymphadenopathy
  3. Elephantiasis (long standing lymphedema)
  4. Eosinophilia
111
Q

What type of transmits loa loa? wuchereria bancrofti?

A

loa loa: Deer fly

wuchereria bancrofti: mosquito

112
Q

What chromosome is CFTR located on?

A

Chromosome 7

113
Q

Name the (5) mutation classes for CF. Which is most common and what is the genetic change associated with it?

A
  1. No synthesis
  2. No maturation (destroyed before proper packaging) * most common - F508 mutation
  3. Blocked regulation
  4. Dec. Cl- conductance
  5. Dec. abudance of CFTRs
114
Q

Name the (2) theories of ASL defect associated with CFTR

A

Airway Surface Liquid

  1. ASL low volume (leads to mucus stasis)
  2. ASL too salty (salty sweat)
115
Q

What are the GI symptoms of CF?

A
  1. Meconium Ileus (black, tarry meconium)
  2. Hypoplastic gall bladder
  3. Focal biliary cirrhosis
  4. Fatty liver
116
Q

Pancreatic effects of CF

A

Duct obstruction due to inspissated (thickened) secretions, which leads to dilation, destruction and fibrosis.

117
Q

98% of men with CF are…

A

Infertile

118
Q

Quantitative pilocarpine iontophoresis is also known as…

A

A sweat test (for CF)

119
Q

What is the antibiotic that is nebulized for CF patients? What are the mucolytics used by CF patients?

A

antibiotic: tobramycin
mucolytics: rhDNAse

120
Q

What role do potentiators play in CF? What is its name? What are the chaperones names?

A

Used to deal with class 3 CF by shifting the CFTR to proper position for use. Ex. Ivacaftor

Chaperone ex. is Lumacaflor

121
Q

Eggshell calcifications in cysts on liver CT is associated with what?

A

Echinococcus granulosus

122
Q

Describe the pain associated with pancreatitis (acute/chronic)

A

Epigastric abdominal pain that radiates to the back

123
Q

What is the presentation of acute cholecystitis

A

Right upper quadrant pain, often radiating to right scapula.

124
Q

Choledocholithias? Cholangitis?

A

Choledocholithias- presence of stones w/in biliary tree

Cholangitis- Acute inflammation of the bile ducts. Includes ascending infection (usually bacterial)

125
Q

Murphy Sign

A

An arrest in inspiration during direct palpation of the right upper quandrant. Associated with acute cholecystitis.

126
Q

Bile stone ileus

A

Impacttion of a gallstone in the intestine (usually a large stone which enters through a cholecystoeteric fistula).

127
Q

Acalculous Cholecystitis

What is it? What does it result from? Who does it affect and how?

A

Acute cholecystitis w/o gallstones. Results from bladder ischemia. Usually seen in patients hospitalized w/ other serious conditions and has a high mortality rate.

128
Q

Porcelain gallbladders are particularly prone to developing…

A

Gallbladder cancer (adenocarcinoma)

129
Q

Cholangiocarcinoma?

What % is extahepatic? Intrahepatic?

A

Cancer of the biliary tree. 90% is extrahepatic; 10% is intrahepatic

130
Q

What is ballooning degeneration and what diseases processes is it associated with?

A

Swelling of hepatocytes

Associated with acute hepatitis, acute drug injury, steatohepatitis (EtOH), and NASH

131
Q

What is feathery degeneration and and what diseases is it associated with? (1)

A

Retains biliary material in swollen hepatocytes

Disease: chronic cholestasis disorders

132
Q

Macrovesicular vs Microvesicular Steatosis

A

Both are accumulation of fat droplets in hepatocytes

Macro (displaced nucleus): associated w/ EtOH, NASH, HCV and diabetes

Micro (no displaced nucleus): acute fatty liver of pregnancy, reyes, valporic acid

133
Q

Key marker(s) of liver cancer? pancreatic cancer? CRC?

A

Liver: AFP (alpha-fetoprotein)

Pancreatic: CA19-9 and CEA

CRC: CEA only

134
Q

Name the liver diseases in which AST is greater than ALT (3)

A

AWA-lem

Alcohol

Wilson’s

Advanced Fibrosis

135
Q

Causes of extremely elevated aminotransferase levels (> 1000u/l) (5)

A

Dark CASA

  1. Drug/toxin induced injury [usually acetaminophen] (not alcohol alone)
  2. Common bile duct obstruction
  3. Acute viral hepatitis
  4. Shock liver
  5. Autoimmune
136
Q

Key markers for cholestasis (4)

Which is most specific to the liver?

A
  1. Alkaline phosphatase
  2. GGT
  3. 5’ nucleotidase (most specific to liver)
  4. Bilirubin
137
Q

What (3) things define acute liver failure?

A
  1. Sudden loss of hepatic fxn in person w/o evidence of preexisting liver disease
  2. Coagulopathy (INR > 1.5) AND
  3. Hepatic encephalopathy
138
Q

When would see this image? What is it called?

A

It’s Chicken wire fibrosis aka pericellular fibrosis.

Associated with alcohol/ non-alcohol liver disease

139
Q

How do the splanchics respond to cirrhosis?

A

Autoregulatory vasodilation and angiogenesis

140
Q

What is the end result for most patients with Hep B? Hep C?

A

Hep B: Full recovery (as healthy state carrier)

Hep C: Transition to chronic

141
Q

How is Hep E spread? Where is it endemic? Likely to become cancer?

A

Fecal-oral

Tropical/subtropical countries

Unlikely risk of cancer

142
Q

What are the non-viral etiologies for chronic hepatitis? (4)

A
  1. Autoimmune (most common)
  2. Drugs
  3. Wilson’s disease
  4. a-1 AT deficiency
143
Q

Staging of hepatitis tells us what? Grading?

List the stages.

A

Staging = degree of fibrosis

Grading= degree of inflammation

Stages:

  1. Portal
  2. Periportal
  3. Bridging
  4. Cirrhosis
144
Q

What do you give to counteract APAP in APAP-related liver injury?

A

NAC

145
Q

Describe the pathogenesis for Alcohol-related liver disease. What are (3) key findings? What is the key complication

A

Acetaldehyde (alcohol metabolite) causes damage to cells. Characterized by:

  1. Swelling of hepatocytes w/ formation mallory bodies
  2. Necrosis
  3. Acute inflammation

Can lead to cirrhosis

146
Q

What are the key risk factors for Non-alcoholic Fatty Liver Disease (NAFLD)?

What is the general pathology and what can it lead to?

A

Associated w/ obesity (dyslipidemia/hyperinsulinemia/insulin resistance) and metabolic syndrome.

These patients have Non-alcoholic steatohepatitis (NASH) which can progress to cirrhosis

147
Q

What is the cause of primary hemochromatosis? Secondary?

How does it present?

What association w/ cancer?

A

Primary: mutation in the HFE gene (usually C282Y)

Secondary: Transfusion/hemolysis

Presents w/ classic triad of cirrhosis, secondary DM and bronze skin

200x inc. HCC risk in setting of cirrhosis.

148
Q

What is the key defect associated with Wilsons disease? Treatment?

A

Autosomal recessive defect (ATP7B gene) in ATP-mediated hepatocyte copper transport.

Results in loack of copper transport into bile and lack of copper incorporation into ceruloplasmin, allowing it to build up into hepatocytes.

Treat w/ D-penicillamine (copper chelation)

149
Q

Sinusoidal Obstructive Syndrome (Veno-Occlusive Disease)

Pathophysiology?

Etiology?

Sx (triad)?

Dx?

A
  • Toxic injury to the sinusoidal endothelium w/ resulting fibrotic occlusions of small hepatic veins
  • Caused by 1. BM transplant, 2. chemo, 3. drugs (ex. azathioprine for immunosuppresion)
  • Sx.: hepatomegaly, ascites, jaundice
  • NO BIOPSY! T__oo dangerous
150
Q

Defining features of focal nodular hyperplasia (FNH)

A

Central stellate scar!

No malignant potential, surgery not recommended, product of long term BC or steroid use

151
Q

What is Nodular Regenerative Hyperplasia and what causes it? (4)

A

Widespread transformation of the hepatic parenchyma into small regenerative nodules w/o fibrosis. Can lead to Non-cirrhotic portal HTN.

Associated w/…

  1. Solid organ transplant
  2. BM transplant
  3. Vasculitis
  4. HIV
152
Q

Describe a Hepatic Adenoma

Who is it common in?

A

A mass (difficult to distinguish from cancer), where the cords of normal hepatocytes while portal tracts (triads) are absent.

Common in young women on BC

153
Q

What are the Sx w/ Hepatic adenoma? Tx?

A

Sx.: Solitary lesion w/ very rare risk of rupture and rar transformation to HCC.

Dx. Discontinue BC and resect, only, if greater than 5cm (inc. transformation risk)

154
Q

Hemangioma

A

Most common benign tumor

155
Q

Angiosarcoma

A

Most common primary sarcoma of the liver– highly aggressive.

156
Q

Hepatoblastoma

What is it? Sx? Types?

A

Most common primary malignant liver tumor of childhood.

Sx: Abdominal enlargement w/ RUQ mass; elevated AFP

Types: Epithelial type and mixed epithelial/mesenchymal

157
Q

What are the (5) overall causes for Hepatocellular Carcinoma (HCC)?

A
  1. Cirrhosis of any cause
  2. Chronic Hep B (w/ or w/o cirrhosis)
  3. NASH
  4. Aflatoxin (food contaminents)
  5. Hereditary Tyrosinemia (highest risk– 40%)
158
Q

Describe the gross presentation of HCC

A

Single lesion, multifocal, and diffusely infiltrative

path: Accumulation of mutations due to repeated cycles of cell death and regeneration. Or integration of viral DNA (HBV)

159
Q

Describe the Fibrolamellar variant of HCC

A

Found in younger people, this form of HCC is not associated w/ cirrhosis and has a moderately better prognosis.

160
Q

What is a Cholangiocarcinoma? What is the largest risk factor? What are the two general categories?

A

Malignancy of the bile ducts

Main factor is primary sclerosing cholangitis (PSC).

Can be intrahepatic (10%) or extrahepatic (90%)

161
Q

Klatskin tumor

A

A particular variant of extrahepatic cholangiocarcinoma in which the perhilar/ hilar region of the biliary tree is blocked. Causes severe jaundice.

MHD 2- Exam 1 (1 decks)

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