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GI Block - Random Factoids > Course Guide High Yield > Flashcards

Course Guide High Yield Flashcards

1
Q

PARASITIC PROTOZOA

A

one celled organisms with a facultative anaerobic metabolism, free oxygen being limited in the host.

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2
Q

“flask-shaped” lesions

A
  • Entamoeba histolytica* is the causative agent of amebic dysentery
  • trophozoites attach and invade intestinal mucosa causing the formation of amebic ulcers in the large intestine primarily in the cecum or sigmoidorectal area, appendix and ascending colon less frequently
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3
Q

“ground glass” cytoplasm and a single
nucleus with central karyosome and evenly distributed chromatin

What do cysts look like?

A

Entamoeba histolytica

cysts are spherical with 1 to 4
nuclei, and may contain sausage
shaped chromatoid bodies.

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4
Q

Acanthamoeba

A
  • free-living protozoans
  • associated with improperly sterilized contact lenses
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5
Q

Naegleria fowleri

A
  • free-living amoeba is found in warm fresh water
  • primary amebic meningoencephalitis
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6
Q

most common intestinal protozoan infection in US

A

Giardia lamblia-a flagellate

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7
Q

cyst is football-shaped with 2-4 nuclei (each cyst with 2 individuals) and axonemes.

A

Giardia lamblia

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8
Q

-oval-pear-shaped trophozoites, with one nucleus

motile by four flagella, and characteristic undulating membrane

A

Trichomonas vaginalis- common sexually transmitted flagellate

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9
Q
  • Oocysts are tiny (4-6 um) and round
  • acid fast nature helps to identify in stained preparations.
A

Cryptosporidium sp.-

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10
Q

Cyclospora cayetanensis:

A

Similar to Cryptosporidium (except larger)

Also acid fast oocysts

Contaminated food (fruit) from South America, Asia

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11
Q

Isospora belli

A

In US, major problem is in AIDS patients. Diagnostic form is large, oval shaped oocyst, often with 2 embryos. Acid fast.

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12
Q

Balantidium coli:

A
  • only known ciliate to cause human disease
  • Major reservoir is swine
  • similar to Entamoeba histolytica (dysentary), but almost never invades beyond gut wall
  • Cyst is diagnostic and infectious stage
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13
Q

Cestodes

A

tapeworms

  • characterized by bodies with 3 principal features. First a scolex (head) with specialized attachment organs (hooks and/or suckers),
  • second, a neck or immature region giving rise to the
  • third region called a strobila.
  • lack of a digestive tract
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14
Q

Nematodes

A

round worms

basic body plan is a tube within a tube, the outer tube is the body wall, inner tube is the digestive system.

larvae undergo a series of molts (shedding of outer cuticle)

L1 larvae referred to as rhabditiform, L3 larvae are referred to as filariform (infective).

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15
Q

world’s most common parasite

A

Enterobium vermicularis -(pinworm)-affects mostly children

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16
Q

rare autosomal dominant genetic disease

(LKB1/STK11 mutation)

A

PEUTZ-JEGHERS SYNDROME

branching smooth muscle
fibers, proliferated complex glands and increased mucin

mucocutaneous pigmentation,
gastrointestinal hamartomatous polyps and increased risk of malignancies in organs such as colon, pancreas, breast, ovary and testis

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17
Q

Extra-intestinal manifestations include congenital hypertrophy of retinal pigment epithelium (CHRPE), osteomas, epidermal cysts, desmoid tumors and CNS tumors.

A

FAMILIAL ADENOMATOUS POLYPOSIS (FAP)

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18
Q

autosomal dominant germline mutation in one of
the multiple mismatch repair genes (MLH1, MSH2

A

HEREDITARY NON-POLYPOSIS COLON CARCINOMA

Lynch syndrome

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19
Q

most common malignancy of the GI tract

A

COLORECTAL ADENOCARCINOMA (CRC)

third most common malignancy in either gender, and second most common cause of cancer-related mortality

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20
Q

Name 4 drugs that Induction Immunosuppression

A
  • Anti-lymphocyte globulin (ATGAM and Thymoglobulin)
  • Alemtuzumab (Campath)
  • Basiliximab (Simulect)
  • Methylprednisolone
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21
Q

Calcineurin inhibitors

A

Cyclosporine

Tacrolimus

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22
Q

Antimetabolites

A

Azathioprine

Mycophenolate

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23
Q

mTOR inhibitors

A

Sirolimus

Everolimus

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24
Q

Alemtuzumab

(Campath®)

A

Humanized monoclonoal antibody against CD52

Binds to CD52 on lymphocytes, monocytes, macrophages, and natural killer cells, which causes cell lysis

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25
Q

Basiliximab

(Simulect®)

A

BASically, an IL-2 receptor-Inhibitory chimeric (XI) MAB

IL-2 Receptor Blockade - monoclonal antibodies (mAb) against the alpha subunit of IL-2.

Binds to the alpha unit of the IL-2 receptor inhibiting binding of IL- 2 thereby preventing activation of lymphocytes

Similar to Daclizumab

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26
Q

Methylprednisolone

(Solu-Medrol®)

A

Corticosteriods - Blocks cytokine gene expression resulting in a decreased immune response

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27
Q

Tacrolimus (Prograf®, TAC, FK 506)

MOA

Major TOX

A
  • blocking calcineurin - Binds to FKBP and inhibits calcineurin (same mechanism as cyclosporin)
  • Along with Cyclosporine, belongs to NIH
    • NEPHROTOXICITY
    • Neurotoxic
    • Increased cholelithiasis in children
    • Hyperglycemic
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28
Q

Cyclosporine
(Neoral®,
Sandimmune®, CsA)

Major TOX

A

Calcineurin Inhibitor - prevents bindig to transcription factor NF-AT.

This cycle belongs to the NIH

  • Nephrotoxicity
  • Increased cholelithiasis in children
  • Hypertension, hyperglycemia
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29
Q

Mycophenolate
Mofetil (Cellcept®,MMF)

Mycophenolate
Sodium
(Myfortic®,MPA)

MOA

TOX

A

Metabolized to mycophenolic acid in liver. It Acts within B and T lymphocytes to inhibit inosine monophosphate dehydrogenase, involved in GMP synthesis in the de novo pathway of purine synthesis - Decreases DNA synthesis in B and T cells - cellular proliferation is decreased.

Clinical use - Immunosuppresant in transplant patients; autoimmune disorders.

GI intolerance, bone
marrow suppression

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30
Q

Azathioprine

Major TOX

(Imuran®, AZA)

A

Anti-Metabolites Inhibits proliferation of T and B cells by preventing RNA and DNA synthesis

GI intolerance, bone
marrow suppression,
_elevated liver
transaminases_

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31
Q

Sirolimus

TOX

(Rapamune®)

A

mTOR Inhibitors - Binds to FKBP-12 forming a complex that inhibits the target of rapamycin which proliferation of T and B-cells

  • Anemia
  • impaired wound
  • healing
  • proteinuria
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32
Q

Everolimus

TOX

(Zortress®)

A

mTOR Inhibitors - Binds to FKBP-12 forming a complex that inhibits the target of rapamycin which proliferation of T and B-cells

  • Anemia
  • impaired wound healing
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33
Q

Glycopyrrolate MOA

A

Anti muscarinic - Block direct muscarinic stimulation of parietal cells, decreasing acid

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34
Q

Sucralfate (Carafate)

A

Cytoprotective - Polymerizes into a protective gel to protect against gastric acid

Gel inhibits back diffusion of H+ and reduces pepsin activity

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35
Q

Cisapride MOA

A

Prokinetic - facilitates ACh release

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36
Q

2 Approved treatments for H. Pylori

A

2 approved treatments

  • Bismuth subsalicylate (Pepto Bismol), metronidazole and tetracycline (2 antibiotics) for 14 days
  • Omeprazole and clarithromycin for 14 days
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37
Q

Metoclopramide

A

cholinomimetic agent and a D2 receptor blocker

Promotes the release of acetylcholine from
myenteric neurons - Increases LES pressure and relaxes pyloric sphincter

Use: Diabetic gastroparisis and GERD

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38
Q

Under restricted use due to association with torsades de pointes

A

Cisapride
– Facilitates acetylcholine release from myenteric plexus

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39
Q
  • Mg citrate
  • Sodium Phosphate
A

Osmotic/ (Saline)

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40
Q

Docusate

A

Surfactant - Sm & large Intestines, Detergent: facilitates mixture of fat and water to soften stool

For painful hemorrhoids
Used to prevent constipation,
only a weak stimulant
Commonly given to
hospitalized pts to minimize
straining

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41
Q

Bisacodyl

A

Stimulant - Colon, Stimulate smooth Ms peristalsis.

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42
Q

Diphenoxylate (with Atropine-Lomotil)

A

Antidiarrheal

meperidine (related piperidine opioid)Acts at mu receptors on enteric neurons

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43
Q

Loperamide (Imodium)

A

Does not cross the BBB

Increase transit time, antidiarrheal

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44
Q

Bismuth Subsalicylate (Pepto Bismol)

A

Salicylate is involved in anti-motility, anti-secretory, anti inflammatory effects

salicylate so Reyes’ syndrome warnings also apply

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45
Q

hepatitis shows greater predisposition to hepatocellular
carcinoma with or without cirrhosis.

A
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46
Q

ground glass hepatocytes

A

containing HBsAg) may be seen

Chronic HBV

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47
Q

Family that HBV belongs to

A

Hepadnavirus

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48
Q

% Adults with HBV that don’t resolve?

A

10% persistent infection

90% Resolve

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49
Q

% of newborn HBV infections that don’t resolve

A

30-90% of newborn infections (from exposure to infectious maternal blood) result in chronic infection

  • immune system is not fully formed
  • vaccination at birth can prevent infection
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50
Q

used as marker for active replication in HBV

A

HBeAg (e antigen) - soluble, not associated with virion

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51
Q

DNA genome of HBV

A

partially double stranded in the virion.

3.2 kb DNA; smallest DNA virus genome

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52
Q

HDV Genome

A
  • Genome is small, single strand RNA, circular
  • Genome contains a ribozyme (RNA) sequence that cleaves the long RNA into unit length pieces and ligates the ends to recreate a circle.
  • Similarities to plant viroids
  • Needs HBsAg coat to make infectious particles
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53
Q

Hepatitis A virus:

Family

Genome

A

Picornaviridae

ssRNA (+)

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54
Q

Hepatitis B virus

Family

Genome

A

Hepadnaviridae (DNA)

partially ds DNA

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55
Q

Hepatitis C virus

Family

Genome

A

Flaviviridae

ssRNA (+)

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56
Q

Hepatitis D virus

Family

Genome

A

Viroid (depends on HBV)

circular ssRNA (-)

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57
Q

Hepatitis E virus

Family

Genome

A

Hepevirideae

ssRNA (+)

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58
Q

Hepatitis viruses that have a ssRNA(+) Genome

A

“ACE in the ssReally Positive”

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59
Q

Causes chronic hepatitis (85% of infections)

A

Hepatitis C virus

Can progress to cirrhosis, then to liver failure, or carcinoma

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60
Q

HCV was THE major cause of post-transfusion hepatitis after HBV was removed from the
blood supply

What was done to solve this problem?

A

HCV antigen is now used to detect anti-HCV antibodies in blood supply:
has eliminated HCV contaminated blood and most post-transfusion hepatitis

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61
Q

Treatment for HCV

A

alpha-interferon for 6 months
40% of patients: ALT levels decrease to normal during therapy
10% to 30% have long-term response/resolve the infection
Many side effects

Interferon + ribovirin: allows lower dose of interferon, fewer side-effects

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62
Q

mortality in pregnancy, up to 25% (3rd trimester infections)

A

Hepatitis E virus

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63
Q

PARTIAL MUCOSAL INVASION

Organisms

Clinical illness

A

Ingested organisms divide and attach to mucosa. Cause
mucosal ulcerations but invade no deeper.

Shigella, Campylobacter jejuni, Clostridium difficile, invasive E.
coli, Entamoeba histolytica

Incubation period is 2-4 days. Dysentery with blood and pus in stools. Of all infectious diarrheas, these are most associated with grossly bloody stools

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64
Q

TOXIN MEDIATED DIARRHEA

Organisms

Clinical Illness

A

Toxin produced by organism, organism does not invade
and may not even be ingested

Vibrio cholera, enterotoxigenic E. coli, Staphylococcus aureus, Bacillus cereus, Clostridium perfringens

Acute, short incubation (2-24 hours), watery diarrhea. Minimal local inflammatory response (0 or few RBCs/WBCs in stool) and usually no fever. Typically, last 2-5 days. Major risk is dehydration.

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65
Q

COMPLETE MUCOSAL INVASION

Most often site?

Organisms?

A

Ingested organism attaches and invades full thickness of
bowel, into regional lymphatics, and occasionally into bloodstream

Site - Colon

  • Salmonella typhi, Yersinia*
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66
Q

Viral agents that cause viral diarrhea

A

Norwalk virus
Norovirus
Rotavirus
Adenoviruses

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67
Q

Reoviridae

Shape?

Gemone

Important members

A
  • icosahedral, double capsid, no envelope
  • double-stranded RNA, segmented (10, 11, or 12)
  • ROTAVIRUS
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68
Q

Rotavirus

  • Transmission*
  • Highest incidence*
  • Incubation*
  • Symptoms*
  • Important for recovery?*
A
  • Major cause of gastroenteritis in infants and a significant cause of mortality of infants in developing countries (1 million fatalities/yr). Age <2 yr, usually.
  • Fecal-oral transmission
  • Highest incidence in fall and winter (November – April)
  • Incubation period: 24-72 hours
  • Symptoms: vomiting, diarrhea, fever, dehydration.
  • IgA is important in recovery, prevention

Therapy - rehydration, the diarrhea usually resolves in 2-7 days. Failure to rehydrate may lead to death, especially in infants. Live attenuated oral vaccine recently approved, now recommended for all infants.

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69
Q

Adenovirideae

  • Important serotypes*
  • Structure*
  • Genome*
  • Disease*
A

Adenovirus serotypes 40, 41, 42 [Serogroup F]

Icosahedral, No envelope

Linear, double-stranded DNA genome

Serotypes 40, 41, and 42 cause acute viral gastroenteritis (fecal-oral spread) in infants
(usually under 1 yr old), often associated with a concurrent respiratory tract infection.

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70
Q

Caliciviridae

  • Shape*
  • Genome*
  • Transmission*
  • Disease*
  • Incubation*
A

Norovirus

no envelope - icosahedral

Positive single strand RNA genome

Food-borne/Fecal-oral

Causes nonbacterial gastroenteritis in school-age children and adults

Incubation period: short – 6-24 hours

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71
Q

How are viral gastroenteridites different from invasive bacterial GI infections?

A

All viral gastroenteridities cause watery diarrhea without blood or WBCs in the stool. Invasive bacterial GI infections (Campylobacter, Salmonella, Shigella) are characterized by GI inflammation, with blood and pus (WBCs) in stool (at least in serious cases) and always fever. Fever may be absent in viral diarrheas.

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72
Q

most common cause of liver disease in the United States

A

NON-ALCOHOLIC FATTY LIVER DISEASE (NAFLD OR
NASH)

rising in incidence.

73
Q

ALPHA-1 ANTITRYPSIN DEFICIENCY

Inheritance

Characterized by:

A

Autosomal recessive disorder of protease inhibitor alpha-1 antitrypsin (from normal PiMM to PiZZ).

presence of eosinophilic round large granules in the cytoplasm of hepatocytes that are PAS positive and diastase resistant

74
Q

FOCAL NODULAR HYPERPLASIA (FNH) OF LIVER

A

incidentally detected mass in young and middle aged
women with a central stellate scar.

abnormal large vessels and the surrounding
liver shows cirrhosis-like nodularity and cholangiolar
proliferation at the interface.

75
Q

men may occur with the use of anabolic steroids

A

HEPATOCELLULAR ADENOMA

76
Q

Second most common primary malignant tumor in the liver

Risk factors

Comparison to prognosis of HCC?

A

CHOLANGIOCARCINOMA

Risk factors include biliary diseases such as primary sclerosing cholangitis, congenital biliary diseases, cirrhosis and toxins
(West) and liver fluke parasite (Far East)

More aggressive than hepatocellular carcinoma with poor prognosis.

77
Q

4th leading cause of cancer deaths in the US

A

PANCREATIC CARCINOMA

78
Q

Alkaline phosphatase

Location?

Function

When elevated?

A

▪ Located on the canalicular surface
▪ Responsible for transport of bilirubin into bile
▪ Elevations seen in obstructive diseases
− Normal (children)
− Fracture

79
Q

Lactate dehydrogenase (LDH)

A

▪ Glycolytic enzyme found in nearly all cells
▪ Five “isoenzymes” forms, LD1 – LD5
▪ LD5 found in hepatocytes, has a short t ½ and not markedly elevated in liver
disease
▪ LDH elevations are usually from heart, RBCs or tumors

80
Q

Gamma glutamyltransferase (GGT)

A

▪ Located on canalicular surface and in microsomes
− Drug inducible
**▪ Not found in bone **− Used to differentiate elevation in ALP of bone and liver origin
▪ ALP and GGT are both elevated in cases of obstructive disease due to their location on canalicular surface of hepatocytes

81
Q

SERMs

A

Raloxifene

Tamoxifen

Toremifene

82
Q

Aromatase Inhibitors:

A

Anastrozole

Exemestane

Letrozole

83
Q

Gonadotropin Releasing Hormone Agonists (synonymous with LHRH agonists):

A

o Goserelin
o Histrelin
o Leuprolide
o Triptorelin

84
Q

Anti-androgenic Agents:

A

Bicalutamide

o Flutamide
o Nilutamide
o Abiraterone
o Enzalutamide

85
Q

Fulvestrant

Degarelix

A

Estrogen Receptor Antagonist

Gonadotropin Releasing Hormone Antagonists

86
Q

used to treat tamoxifen induced hot flashes

A
87
Q

Raloxifene (Evista®)

A

SERM - receptor antagonist in breast and agonists in bone. Does not increase the risk of endometrial carcinoma because it is an endometrial antagonist.

perfectly safe for woman with intact uterus that wants to go on for prevention. (endometrial antagonist) Tamoxifen is partial agonist.

88
Q

Prednisone Toxicity

A

“COACH PP says HI, wants you to take roids, (drinking pepsi, must be psychotic)”:

  • Cushingoid features;
  • Osteoporosis;
  • Acne;
  • Cataracts;
  • Hyperglycemia/DM;
  • Psychosis;
  • Peptic ulcer;
  • HTN;
  • Insomnia.

If on prednisone for >3 months start prophylaxis bisphosphonate to prevent osteoporosis.

89
Q

Toremifene (Fareston®)

A

Has shown no advantage over tamoxifen in treatment of breast cancer

90
Q

Toxicities of SERMs:

A
  • Hot flashes
  • Nausea and vomiting
  • Edema
  • Thromboembolism
  • Endometrial cancer
91
Q

Treatment of breast cancer in premenopausal women

A
92
Q

Treatment of Breast cancer in postmenopausal women

A
  • An AI needs to be incorporated somewhere in the therapeutic regimen
  • Endocrine agents are always given sequentially after chemotherapy
93
Q

second-most common
type of secretory pituitary adenoma

A

Growth Hormone (somatotroph adenomas

40% have GNAS1 mutation (prevents GTPase activity on Gsα

94
Q

Cushing syndrome

vs.

Cushing disease

A

hypercortisolism

95
Q

Nelson’s syndrome

A

Development of large ACTH secreting adenoma after
removal of both adrenal glands for Cushing syndrome. No hypercortisolism develops because of lack of adrenals. Patients present with mass effect and hyperpigmentation.

96
Q

Pituitary apoplexy

A

hemorrhage into pituitary gland, usually into a large adenoma

▪ Symptoms of headache, diplopia and hypopituitarism
▪ Neurosurgical emergency

97
Q

Lymphocytic hypophysitis

A

Inflammatory lesion of AP gland

More common in women, especially peripartum
− Partial or total pituitary hypofunction
− Lymphoplasmacytic infiltrate of gland
− Causes pituitary hypofunction, occasionally headaches and visual field defects
− Autoimmune theory hypothesized

98
Q

Craniopharyngioma

Types

Prognosis

A

HYPOTHALAMIC SUPRASELLAR TUMORS

  • Adamantinomatous - Cysts filled with dark brown fluid (motor oil) and cholesterol crystals, +keratin, Local invasion brain
  • Papillary - no keratin, cysts or motor oil

Good prognosis

99
Q

Pineoblastoma

Pineocytoma

A

Constitute 45% of all pineal tumors

Typically found in children within the first two decades
of life

Pineocytoma - rare tumore

100
Q

Sulfonylureas

Names

MOA

TOX

A

1st - TOLBUTAMIDE, CHLORPOPAMIDE

2nd - GLY–IDE - GLYburIDE, GLImeprilIDE, GLIpizIDE

MOA - 3 main mechanisms

KATP channel blockade - In pancreatic beta-cells, this decreases K+ efflux, increasing intracellular K+ depolarizing the cell membrane and activating VDCC, augmenting Ca2+ influx that promotes insulin secretion

  1. Stimulate insulin release - (Potassium channel)
  2. increase insulin action on target tissues by prolonging binding of insulin to target receptors
  3. reduce serum glucagon levels

TOX - Hypoglycemia

101
Q

Metformin

A

METabolic FORMation of glucose is INhibited in the liver

biguanide

  • INHIBITS HEPATIC GLUCONEOGENESIS and, thus, decreases hepatic glucose output
  • INCREASING PERIPHERAL UTILIZATION OF GLUCOSE (increasing insulin sensitivity) by adipose and skeletal muscle
  • DECREASES Glucose absorption from GIT
  • serious adverse effect of metformin is lactic acidosis; GI upset
102
Q

Acarbose, Miglitol

A

A CAR from BOSE nd a MIG LITTLE Block glucOSE absorption in the intestin by inhibitng alpha-glucosidase and only a LITTLe glucose can MIGrate across the intestine via GLUT-5

Alpha-glucosidase Inhibitors - Alpha-glucosidase is an enzyme that is bound to the jejeunal brush border, and cleaves oligo to monosaccharides that are rapidly absorbed. These drugs are competitive inhibitors of the enzyme, and will delay but not prevent the absorption of the monosaccharide glucose.

Acarbose was the first available alpha-glucosidase inhibitor. Miglitol now available.

103
Q

Sitagliptin/Saxagliptin

A

dipeptidyl peptidase‐4 (DPP‐4) inhibitors

GLP-1 secretion is deficient in type 2 diabetes. A class
 of agents has been developed which **inhibit DPP-4** and thus **restore GLP-1** levels to normal. This has been shown to reduce blood glucose levels in type 2 diabetes with the same potency of other available oral agents.
104
Q

Most common combination treatment for DM II

A

a drug to simulate insulin secretion, i.e., one of the sulfonylureas or a DPP-4 inhibitor with metformin. This regimen is highly effective and has an extensive clinical
experience.

105
Q

MEN I, or Werner Syndrome

A
  • Autosomal Dominant Trait
  • The three P’s
    ▪ Parathyroids (primary hyperparathyroidism)
    ▪ Pancreas, endocrine tumors (gastrinomas)
    ▪ Pituitary gland (prolactinoma)
106
Q

Zetia (Ezetimibe)

A
  • Transport inhibitor - blocking the absorption of cholesterol by the brush border cells of the intestine.
  • Used to reduce LDL.
107
Q

Potency of statins

A

From Most to least = RASP

Lovastatin (mevacor) is prototype

  • Rosuvastatin (Crestor)
  • Atorvastatin (Lipitor)
  • Simvastatin (Zocor)
  • Pravastatin (Pravachol)
108
Q

Nicotinic acid (Niacin)

MOA

What is the biggest advantage of this drug?

A

 Much higher dosage, 1-3g, is used for hypolipidemic effect. Vitamin dose is only 20 mg.
 Niacin is rapidly absorbed and eliminated by renal clearance.
 Note: The acid form of the drug, Niacin or nicotinic acid, is active. The basic form of the drug, niacinamide or nicotinamide does not have hypolipidemic action.

MOA Decreasing lipolysis of adipose thus decreasing VLDL and LDL production and secretion.

 Most effective agent for INCREASING HDL 15%-35% decrease LDL levels

109
Q

Gemfibrozil/Clofibrate

MOA

Main use

Adverse effects

A

Fibrates include ciprofibrate, bezafibrate, fenofibrate

  • Decrease Fatty acid synthesis, and stimulate lipoprotein lipase-enhanced hydrolysis of TGAs into VLDL and chylomicrons
  • Stimulates synthesis of apoA-1 (Gemfibrozil)
  • Main use - decrease TG 20-50%
  • DO NOT COMBINE WITH STATINS!
110
Q

Vytorin

A

Statin and Ezetimibe (Zetia): This combination, Ezetimibe and simvastatin

the combination may be used to reduce potential side
effects of the statins by allowing for a lower dose of the statin drug to be used to obtain a specific reduction
in cholesterol

111
Q

Optimal LDL level

Total cholesterol

A

Identifies LDL cholesterol ,< 100 mg/dL

Total cholesterol <200 desirable, >240 is High

112
Q

Major Risk factors that modify LDL goals

A

Smoking

HTN

Low HDL

Family history

Age

113
Q

Incidence of Thyorid Carcinomas

A

▪ Papillary carcinoma (>85%)
▪ Follicular carcinoma (5 – 15%)
▪ Medullary carcinoma (5%)
▪ Anaplastic carcinoma (< 5%)

114
Q

Primary hyperparathyroidism incidence

A
115
Q

Rosiglitazone

SD

MOA

CU

TOX

A

Similar drugs - thiazolidinediones include pioglitazone and troglitazone

MOA - binding to PPAR-gamma, results in upregulation of multiple genes that decrease insulin resistance

CU - non-insulin dependent type 2 diabetes

TOX - Hypoglycemia; edema; liver damage (troglitazone - withdrawn)

116
Q

Atorvastatin

A

Similar drugs - HMB-CoA reductase inhibitors include pravastatin, lovastatin, rosuvastatin, simvastatin, fluvastatin

MOA - Inhibit HMG-CoA reductase and increase the concentration of LDL receptors on hepatocytes, incresing the liver’s ability to extract LDLD and VLDL from the serum.

CU - decrease total cholesterol and LDL levels. TG mildly decrease with this drug

SE - Myopathy; abnormal liver function tests; teratogen

Ezetimbe is a cholesterol-lowering medication that decreases cholesterol absorption from the GI tract - decrease in LDL levels

117
Q

Cholestyramine

A

Similar drugs - bile acid resins - colestipol and colesevelam

MOA - inhibit reabsorption of bile acids in jejunum and ileum

CU - decrease LDL levels

SE - GI upset, bile stone risk

118
Q

Treatment of hyperthyroidism

Treatment of hypothyroidism?

A

Propylthiouracil - Similar drugs - Methimazole

MOA - inhibits thyroid peroxidase, enzyme involved in organification, by coupling iodotyrosines - results in inhibition of thyroid hormone synthesis in thyroid and inhibiting peripheral conversion of T4 to T3.

CU - hyperthyroidism

Levothyroxine is synthetic form of T4 (thyroid hormone) used to treat hypothyroidism

119
Q

Flutamide

A

MOA - competitive antagonist at the androgen receptor - decreasing growth effects of testosterone on prostate. Body detects low testosterone and increases serum LH. Because LH increases, flutamide is always administered with leuprolide

CU - prostate cancer

Danazol - mild agonist at androgen and progesterone receptors - treat endometriosis.

120
Q

Leuprolide

A

Similar drugs - nafarelin and goserelin

MOA - GnRH agonist - initial increase in LH and FSH when first administered, eventually downregulates receptors and LOW LH and FSH ensue.

CU - metastatic prostate cancer, leiomyomas, treatment of infertility when administered intermittently

SE - impotence, hot flashes

Clomiphene - partial agonist at estrogen receptors in pituitary - inreasing release of gonadotropins

121
Q

Lipoprotein lipase

A
  • Activated by apo C-II - resulting in fatty acid release to heart, skeletal muscle, and mammary glands.
  • Hydrolyzes TAGs in chylomicrons;
  • Stimulated by fibrates (Gemfibrozil) breaking down TAGs into VLDL and chylomicrons which are removed - DECREASE TAGS
  • attached to luminal surface of vasculature of cardiac muscle, skeletal muscle, and adipose tissue.
  • Deficiency results in hyperchylomicronemia (type I hyperlipoproteinemia)
122
Q

Lecithin cholesterol acyl transferase (LCAT)

A

Plasma enzyme that esterifies HDL cholesterol - activated by apo A-1 (Put A1 steak sauce on Cat)

123
Q

Apo B100

A
  • LDL clearance from serum;
  • located on LDLs,
  • mediates VLDL secretion
  • binds to LDL receptor on plasma membrane.
  • Allows extrahepatic tissue to take up cholesterol.
  • Abetalipoproteinemia - hereditary inability to synthesize lipoproteins due to deficiencies in apoB100 and apoB-48
124
Q

Apo B48

A
  • Chylomicron clearance from serum
  • unique to chylomicrons;
  • abetalipoproteinemia - deficiency of apoB48 and apoB100 -can’t export absorbed lipid as chylomicrons
125
Q

2 main causes of esophageal hematemesis

A

lacerations (M-W syndrome)

Varices (cirrhosis)

126
Q

Process occuring

A

Barrett’s Esophagus with low grade and high grade dysplasia (these changes only seen microscopically)

127
Q

Diagnosis?

A

Esophageal adenocarcinoma in the distal esophagus

128
Q

Diagnosis?

A

Autoimmune gastritis is an uncommon cause of chronic gastritis (<10%)

Autoantibodies against parietal cells and intrinsic factor This causes hypochlorhydria and anemia

129
Q

Type of disease in top image vs. bottom?

A

Gastric carcinoma - Localized or intestinal type

Gastric carcinoma - Diffuse infiltrating (linitis Plastica)

130
Q

Type of cancer in each? Characteristics?

A

Intestinal type shows gland formation on top

  • Male>female 2:1
  • 50-60s
  • H pylori or BE
  • localized mass
  • geographic variation

Diffuse infiltrating shows signet ring cells on bottom

  • Male=female
  • 40s
  • unknown
  • no geographic variation
131
Q

most common location for extra-nodal lymphomas

A

GI tract is the most common location for extra-nodal
lymphomas and stomach is the most common GI site

132
Q

Characteristic volcano-like ulcer exudates

A

Pseudomembranous Colitis

Characteristic volcano-like ulcer exudates (endoscopically pseudomembranous).

133
Q

Compare MOA of cyclosporin and Tacrolimus

Which is more potent?

A

Cyclosporine binds cyclophilin

Tacrolimus binds FKBP-12

(both are calcineurin inhibitors)

Tacrolimmus more potent

134
Q

Potency of immunosuppresants by class

A

CNIs (Tacrolimus, Cyclosporine) >

mTOR Inhibitors (Siroliums, Everolimus) >

Antimetabolites>

Corticosteroids

135
Q

specific polymorphism
in NOD2 (nucleotide oligomer binding domain 2) gene
Caucasians of European ancestry

A

Crohn’s

  • Common family history
  • 50% concordance in identical twins
136
Q

Current theories on cause of IBDs

A
  • Abnormal immune (T-cell) response
  • Epithelial defects - Defects in tight junctions (‘leaky gut’)
  • Abnormal response to normal flora
137
Q

What is the disease?

Describe the findings and pathogenesis in each quadrant.

A

Crohns

A - Small intestinal stricture - full-thickness inflammation with knife-like fissures through mucosa, submucosa, muscularis propria and serosa!

B - Linear mucosal ulcers and thickened intestinal wall - full-thickness wall involvement

C - Perforation and serositis - all the way to the serosa! full thickness

D - Creeping fat - extensive fibrosis pulls on the fat that is in the mesentary!

138
Q

$ Describe the Adenoma-carcinoma sequence

A

Describes molecular progression from normal colonic mucosa to adenomatous polyp to carcinoma

  1. APC gene mutation, a tumor suppresor, both copies must be knocked out (sporadic or germline) increase the risk for formation of the polyp
  2. K-ras mutation leads to the formation of the polyp
  3. p53 mutation and increased expression of COX allows for progression to carcinoma
139
Q

Type of polyp

A

adenomatous polyp - neoplastic proliferation of glands, second most common, benign, may probress to adenocarcinoma with the AC sequence.

140
Q

Most common risk factors for HCV infections

A
  1. IV drug abuse (54%)
  2. Multiple sex partners (36%)
  3. Unknown (32%)
  4. Surgery (16%)
141
Q

Tissue type? Injury?

A

Chronic hepatitis ( in this case HCV)

  • Inflammation predominantly involves portal tracts (center with apoptosis of hepatocytes)
  • Less inflammation in lobules
142
Q

Liver biopsy obtained, diagnosis?

Immunostain is positive for what?

A

HBV “ground glass cells”

Immunostain positive for HBsAg

143
Q

What does the liver tissue show?

A

Alcoholic hepatitis - The cluster of inflammatory cells marks the site of a necrotic hepatocyte (arrow).

Swelling of hepatocytes is seen (white)

144
Q

$$$$$ This is the hallmark of what disease?

A

Alcoholic hepatitis - Eosinophilic Mallory bodies are seen in hepatocytes, which are surrounded by fibrous (Masson stain) tissue

  • Mallory bodies - damaged intermediate filaments (cytokeratin filaments) are located inside, necrosis, acute inflammation.
  • Acetaldehyde mediates damage - chemical injury seen in binge drinking
145
Q

Disease process that caused this appearance?

What is blue stain?

A

Alcoholic cirrhosis.

A, The characteristic diffuse nodularity of the surface reflects the processes of nodular regeneration and scarring. The greenish tint of some nodules is due to bile stasis. A hepatocellular carcinoma is present as a budding mass at the lower edge of the right lobe (lower left).

B, The microscopic view shows nodules of varying sizes entrapped in blue-staining fibrous tissue. The liver capsule is at the top (Masson trichrome). - Ischemic necrosis and fibrous obliteration of nodules eventually create broad expanses of tough, pale scar tissue (“Laennec cirrhosis”).

146
Q

How is iron level normally controlled in the body?

A

Level of body iron is normally controlled by
increase or decrease in iron absorption

147
Q

2 ways to create iron overload:

A

Hemosiderosis - deposition of hemosiderin (iron) in tissues.

Hemochromatosis - the disease, abnormal increase in absorption causing organ damage, genetic.

  • Can Cause Deposits - Cirrhosis, CHF,DM
  • Clasic triad: micronodular Cirrhosis +skin pigmentation + Diabetes mellitus
148
Q

Normal total body iron pool

When does disease occur?

A
  • Normal total body iron pool is 2-5 gm (0.5 gm in liver)
  • Disease after 20 gm accumulation
149
Q

Hereditary Hemochromotosis

Age of Presentation

Defect? Inheritance?

A

AR defect in iron absorption (primary)

  • After 40 years
  • mutation 6p21.3 HFE gene (343 aa protein) Cysteine-to-tyrosine substitution at 282 (C282Y) in 70-100% cases
  • Heterozygosity 1 in 9, Homozygosity 1 in 200 (Commonest genetic disease in USA), but only 20% penetrance
    (disease in only 20% of homozygous population)
150
Q

Diagnosis?

What is characteristic in the top image?

The EM image shows which organelle?

A

α1-Antitrypsin deficiency - characterized by the presence of round-to-oval** **cytoplasmic globular inclusions in hepatocytes, which in routine H&E stains are acidophilic and indistinctly demarcated from the surrounding cytoplasm - STRONGLY PAS +

Periodic acid–Schiff (PAS) stain of the liver, highlighting the characteristic red cytoplasmic granules

Electron micrograph showing the dilatation of the endoplasmic reticulum

151
Q

central stellate scar

A

Focal Nodular Hyperplasia (FNH) - Localized vascular alteration (Proliferated arteries around obliterated portal vein branches)

152
Q

Diagnosis?

A

Liver cell adenoma or Hepatocellular adenoma

  • Young women (>30) who use oral contraceptives (>7 yrs use)
  • Rarely men who use anabolic steroids
  • Mistaken for FNH or HCC
  • Risk rupture in pregancy and hemorrhage (20% mortality)
153
Q

Most common etiological agent that causes HCC

A

#1 HBV is the most common etiological agent (only 50% cases have cirrhosis)

#2 Aflatoxin (fungus Aspergillus flavus – contaminating peanuts and grains)

154
Q

Diagnosis?

A

Hepatocellular carcinoma. A, Liver removed at autopsy showing a unifocal, massive neoplasm replacing most of the right hepatic lobe in a noncirrhotic liver; a satellite tumor nodule is directly adjacent.

B, Microscopic view of a well-differentiated lesion; tumor cells are arranged in nests, sometimes with a central lumen.

155
Q

Most common histological type of pancreatic cancer?

A

ductal adenocarcinoma

156
Q

Infectious form of diphyllobothrium latum

Diagnostic form?

A

Plerocercoid in undercooked fresh water fish

Operculate eggs (little trap door) or proglottid in stool

157
Q

T. saginata proglottid vs

T. solium proglottid

A

T. saginata Proglottid > 12 uterine branches

T. solium proglottid < 12 uterine branches

158
Q

Thin-walled oval eggs in stool

A

Hookworms - necator americanus and Ancylostoma duodenale

159
Q

Infective Form - Flat-sided, embryonated eggs. Infectious 4 hours after deposit.

A

Enterobius vermicularis (Pinworm)

160
Q

MOA Anti-lymphocyte globulin

A

Complement mediated cell lysis of circulating T-cells

161
Q

MOA of corticosteroids as immunosuppresants

A

Anti-inflammatory response
Reduced production of cytokines (IL-1, IL-2, IL-6, IFN-γ and TNF-α)
Impair monocyte/macrophage function
Decrease the number of circulating CD4+ T cells

162
Q

When would you use an mTOR inhibitor?

A

Delayed graft function (kidney transplant)
Underlying renal insufficiency (heart or lung transplant)
Drug intolerance (all transplants)
Calcineurin toxicity (all transplants, especially kidney)
Pancreas transplant

163
Q

Typical maintenance regimens for Kidney and Liver transpants

A

Tacrolimus + mycophenolate + prednisone

164
Q

Toxicity of Tacrolimus vs Cylosporine?

A

Tacrolimus is more neurotoxic and Hyperglycemic

165
Q

Compare toxicities of Azathioprine and Mycophenolate

A

Mycophenolate can cause diarrhea (++) and azathioprine doesnt. “My diarrhea”

Azathioprine can cause hepatotoxicity (+); mycophenolate does not.

166
Q

Immunosuppresant most likely to cause neurotoxicity?

Hirsutism

Hyperglycemia

A

Tacrolimus > Cyclosporine

Cyclosporine > Tacrolimus

Tacrolimus > Cyclosporine

167
Q

most common nosocomial infectious diarrhea and nosocomial toxic megacolon

Treatment?

A

Clostridium difficile

CDC and SHEA recommend Metronidazole as the first line agent

168
Q

vehicles that transport cholesterol to the artery wall

A

Plasma lipoproteins that contain Apo B100 including LDL, VLDL , IDL

169
Q

most potent compound and used for osteoporosis in post-menopausal women

A

Alendronate

170
Q

Inhibit activity of osteoclasts

A

Bisphosphonates: Alendronate, etidronate, pamidronate

171
Q

inhibitor of bone resorption

A

Calcitonin - has been shown to reduce bone pain from osteoporotic vertebral compression fractures

172
Q

Short acting insulin

Normal

Intermediate

Long acting

A

**Rapid acting: Lispro, Aspart, Glulisine, **3–6 hours

Short-acting: Regular

Intermediate: NPH

**Long acting: Glargine, Detemir **24 hours

173
Q

Alpha fetoprotein

A

Major plasma protein in fetal life (md/dL range)
• Concentration falls postpartum (ng/L)
• Increases in hepatocyte regeneration or proliferation
– Acute hepatitis
– Recovery from hepatitis
– Liver neoplasm

174
Q

Clinical features of cushing syndrome

A
  • Obesity or weight gain (95%)
  • Facial plethora (90%)
  • Rounded face (90%)
  • Decreased libido (90%)
  • Thin skin (85%)
  • Menstrual irregularity (80%)
  • Hypertension (75%)
  • Hirsutism (75%)
  • Depression (70%)
  • Easy bruising (65%)
  • Glucose intolerance (60%)
  • Weakness (60%)
  • Osteopenia or fracture (50%)
175
Q

Treatment for adrenogenital syndromes (hyperplasia of adrenal glands)

A

exogenous glucocorticoids

176
Q

Most common type of adrenocortical carcinomas

A

METASTATIC CARCINOMAS ARE SIGNIFICANTLY MORE COMMON THAN PRIMARY CARCINOMAS

177
Q

Rule of 10s for pheochromocyoma

A

•~90% arise in the medulla
•~10% extra-adrenal location
•~90% are sporadic
•~10% familial
•~10% of sporadic are bilateral
•~10% are biologically malignant
•~10% do not have hypertension

178
Q

Most common pheo associations

A

A.MEN syndromes
B.Type I neurofibromatosis
C.Von Hippel-Lindau disease
D.Familial paraganglioma

179
Q

Frequency of Pituitary Adenoma Types

A
  1. 30% Prolactin
  2. 25% Nonfunctioning (Null Cell)
  3. 20% Growth Hormone

GI Block - Random Factoids (2 decks)

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