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STEP Flash Cards > PT7 > Flashcards

PT7 Flashcards

1
Q

Acute necrotizing pancreatitis pathophysiology

A

Abnormal activation of trypsin within the pancreas - leads to activation of other proteolytic enzymes and subsequent autodigestion

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2
Q

A mutation involving the inactivating cleavage site on trypsinogen would lead to

A

Pancreatitis

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3
Q

Sx of lead poisoning

A

Colicky abdominal pain, headaches, constipation, wrist drop/foot drop (peripheral neuropathy), hypochromic anemia and basophilic stippling

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4
Q

Explain “olive sign” in congenital pyloric stenosis

A

Thought to be a secondary consequence of the hypertrophy of the pyloric muscularis mucosae

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5
Q

Diphenoxylate indication and MOA

A

Opiate anti-diarrrheal; binds to mu opiate receptors in the GI tract to slow motility

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6
Q

Name the 3 reducing sugars

A

Glucose, fructose, galactose

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7
Q

Essential fructosuria

A

AR; asymptomatic disorder; fructokinase deficiency (fructose cannot go to fructose-1-ph and is therefore excreted as fructose in urine)

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8
Q

Galactosemia

A

AR; def. galactose-1-ph uridyl transferase - it is NOT asymptomatic

Sx: neonatal jaundice bleeding diathesis, feeding intolerance, hypotension
Rx: no milk products and soy-based formula

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9
Q

Aldolase B (and def.)

A

Life-threatning; cannot turn F-1-ph into DHAP & glyceraldehyde; treat by eliminating dietary fructose
Sx: after eating fructose foods - failure to thrive, hepatomegaly, cirrhosis

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10
Q

Pompeii disease

A

Acid alpha glucosidase (acid maltase) deficiency - glycogen storage disease
Sx: hepatomegaly, cardiomegaly

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11
Q

Describe V. cholerae organism

A

Gm -
Oxidase +
comma-shaped rod
Can survive on alkaline media

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12
Q

Campylobacter organism

A

Gm -
Oxidase +
Curved, motile rod
CANNOT survive on alkaline media

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13
Q

MOA Cholera bacteria

A

DOES NOT INVADE INTESTINAL EPI; inc cAMP levels by inc activity of adenylate cyclase in intestinal mucosa - this causes increased efflux of sodium and chloride into lumen - massive water loss and watery diarrhea

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14
Q

Consequence of lead overdose

A

Affinity for sulfhydryl groups -ihibits enzymes that incorporate iron into the heme molecule (ex: delta-aminolevulinic acid dehydratase & ferrochetolase)

Delta-aminolevulinic acid formation requires pyridoxal phosphate as a cofactor as well

In lead poisoning, blood and urinary levels of this enzyme are increased

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15
Q

3 main causes of HIV-associated esophagitis

A
  1. Candida
  2. CMV
  3. Herpes
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16
Q

How to differentiate between 3 main causes of HIV-associated esophagitis

A
  1. Candida: grey/white pseudomembrane patches, erythematous mucosa, see yeast cells and pseudohyphae
  2. Herpes: vesicles that evolve into punched out ulcers; see eosinophilic intraneuclear inclusions
  3. CMV: linear ulceration; see intranuclear and cytoplasmic inclusions
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17
Q

Treatment for inflammatory traveler’s diarrhea (stool containing blood and mucus)

A

Cipro, fluoroquinolones

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18
Q

Mebendazole used for

A

Helminths (ex: roundworms like Ascaris, enterobius, ancyclostoma

19
Q

Albendazole treatment for

A

E. granulosus - tapeworm - produces cysts in the liver

20
Q

Loperamide used for

A

Opiate antimotility drug can be prescribed in some cases of traveler’s diarrhea (where there is no fever or blood)

21
Q

Erythromycin used to treat which enteric?

A

Campylobacter jejuni - in lieu of fluoroquinolones

22
Q

How MHC II molecules work

A

ONLY on antigen-presenting cells (ex: dendritic cells, macrophages, B-lymph)

Present EXOGENOUS antigens that have been taken up by phagocytosis and have been degraded by acidification via endosome-lysosome/phagosome-lysosome fusion

MHC II concurrently synth from RER and routed to endosome by golgi - each MHC II has invariant chain bound to its antigen binding site

Fusion of MHC II with acidified endosome containing antigen fragments causes degradation of invariant chain and loading of antigen onto MHC II

This complex then displayed on surface of antigen presenting cell - available to bind TCR on T-lymphocytes

23
Q

How MHC I works

A

On surface of majority of cells in the body - presents ENDOGENOUS antigen/self-antigen/viral antigen

Proteins in cytoplasm are degraded by proteasome and transported into RER where they are loaded onto MHC 1 and together, complex routed to Golgi

NEVER processed within acidified lysosomes

24
Q

Secretory form of IgA

A

Dimer - found in clostrum (aka breast milk)

25
Q

Define gastric erosion

A

Mucosal defects that do not fully extend through the muscularis mucosa (that is, limited to mucosal layer)

26
Q

Gastric ulcer definition

A

Penetrate through the mucosal layer and extend into the submucosa

27
Q

Glutamine-glutamate cycle in the brain

A

Helps to regulate glutamine, glutamate, and ammonia levels in the brain!

Glutamate, produced by neurons (as a NT) can travel into neighboring astrocytes where it is converted to Glutamine via Glutamine synthase (requires ammonia/NH4+) - Glutamine is non-neuroactive

Glutamine then released by astrocytes back into neurons - can either turn into

  1. Glutamate (again) - used as NT
  2. Alpha-ketoglutarate - used for Kreb’s cycle and energy production for neuron
28
Q

Hyperammonia impact on neurons

A

TOO MUCH ammonia will cause excess glutamine to build up in the astrocyte (because ammonia helps glutamine synthase convert glutamate to glutamine)

This depletes glutamate and alpha-ketoglutarate levels in brain in attempts to detox all the excess ammonia

Inc. glutamine causes hyperosmolarity and astrocyte swelling/impairment

Dec. glutamate stores = impaired excitatory neurotransmission (ex: NMDA)

Dec. alpha-ketoglutarate = impaired energy metabolism

29
Q

Heptaic encephalopathy pathophysiology

A

Related to increased circulatory levels of ammonia and other neurotixins due to failure of liver to metabolize waste products

30
Q

Ras-MAP kinase transduction pathway

A

GF ligand binds to receptor tyrosine kinase causing auto-phosphorylation of receptor

Phosphotyrosine produced activates Ras (G-protein)
Activated Ras bound to GTP (inactive bound to GDP) - phosphorylation cascade
Activates MAP kinase - enters nucleus to influence gene transcription

Active Ras inactivated via GTPase-activating protein (GAP) - hydrolysis of GTP to GDP

31
Q

Ras mutation

A

lead to inability to split GTP (inactivate it) - permanently activated Ras stim. cell proliferation and can lead to cancer

32
Q

cAMP transduction pathway involves

A

Protein kinase A

33
Q

cAMP and lac operon

A

LOW cAMP = inactive lac operon - usually means you’re in a glucose environment so you don’t need to metabolize lactose

HIGH cAMP = active lac operon - cAMP binds to CAP protein to form a complex and bind upstream from the promoter region and act as a positive regulator

34
Q

Common pathogen to colonize a perforated appendix that has evolved into an intraabdominal abscess

A

Bacteroides fragilis - common anaerobic, gram-negative bacillus
Favors abscess formation
Common in intraabdominal infections along with E. coli, enterococci, strep

35
Q

HNPCC/Lynch syndrome

A

leads to occurrence of colonic adenocarcinomas at a young age (<50), along with predisposition for extraintestinal malignancies

Involves mutation of DNA mismatch repair genes (NOT mutations in proto-oncogenes or anti-oncogenes seen in sporadic colon cancer)

36
Q

Functions of:

  1. Glycosylase
  2. Endonuclease
  3. Lyase
  4. DNA pol & ligase
A
  1. Glycosylase: cleaves altered base in base excision repair - leaves an AP site
  2. Endonuclease cleaves 5’ end
  3. Lyase cleaves 3’ sugar phosphate
  4. DNA Pol + ligase fill the gap
37
Q

Colonic manifestation of Kaposi’s sarcoma

A

Reddish/violet, flat maculopapular lesions or hemorrhagic nodules - see SPINDLE-SHAPED TUMOR CELLS with small vessel proliferation

38
Q

E. histolytica colonic manifestation

A

Numerous discrete, flask-shaped ulcerative lesions - see trophozoites containing RBC

39
Q

Colonic manifestation of CMV

A

Multiple ulcers and mucosal erosions - CMV cells with inclusion bodies

40
Q

GI complication of opiod analgesics

A

Can cause smooth muscle cells to conract in the sphincter of Oddi - leading to constriction and spasm - can increase common bile duct pressure (potentially lead to biliary colic)

41
Q

What is the protective mechanism behind healthy people not getting C. difficile infections?

A

Intestinal biomass - the sheer number of organisms that colonize the GI system - outcompetes pathogenic bacteria such as C. difficile for nutrients and adhesion sites

That’s why abx treatment can facilitate C. diff infection

42
Q

Typhoid fever presentation

A

Salmonella typhi - associated with history of recent travel to areas where disease is endemic (not industrialized nations) - fecal/oral

Penetrate gut mucosa and survive within macrophages which carry organism aroudn body - hepatosplenomegaly - intestinal hemorrhage, gut perforation

Salmon-colored rose spots on abdomen

43
Q

Mucus diarrhea, cauliflower-like mass in sigmoid colon indicates…

A

Villous adenoma

STEP Flash Cards (14 decks)

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