Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

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

A

Pancreatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Sx of lead poisoning

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Explain “olive sign” in congenital pyloric stenosis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Diphenoxylate indication and MOA

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Name the 3 reducing sugars

A

Glucose, fructose, galactose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Pompeii disease

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe V. cholerae organism

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Campylobacter organism

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

3 main causes of HIV-associated esophagitis

A
  1. Candida
  2. CMV
  3. Herpes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

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

A

Cipro, fluoroquinolones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Define gastric erosion
Mucosal defects that do not fully extend through the muscularis mucosa (that is, limited to mucosal layer)
26
Gastric ulcer definition
Penetrate through the mucosal layer and extend into the submucosa
27
Glutamine-glutamate cycle in the brain
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
Hyperammonia impact on neurons
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
Heptaic encephalopathy pathophysiology
Related to increased circulatory levels of ammonia and other neurotixins due to failure of liver to metabolize waste products
30
Ras-MAP kinase transduction pathway
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
Ras mutation
lead to inability to split GTP (inactivate it) - permanently activated Ras stim. cell proliferation and can lead to cancer
32
cAMP transduction pathway involves
Protein kinase A
33
cAMP and lac operon
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
Common pathogen to colonize a perforated appendix that has evolved into an intraabdominal abscess
Bacteroides fragilis - common anaerobic, gram-negative bacillus Favors abscess formation Common in intraabdominal infections along with E. coli, enterococci, strep
35
HNPCC/Lynch syndrome
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
Functions of: 1. Glycosylase 2. Endonuclease 3. Lyase 4. DNA pol & ligase
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
Colonic manifestation of Kaposi's sarcoma
Reddish/violet, flat maculopapular lesions or hemorrhagic nodules - see SPINDLE-SHAPED TUMOR CELLS with small vessel proliferation
38
E. histolytica colonic manifestation
Numerous discrete, flask-shaped ulcerative lesions - see trophozoites containing RBC
39
Colonic manifestation of CMV
Multiple ulcers and mucosal erosions - CMV cells with inclusion bodies
40
GI complication of opiod analgesics
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
What is the protective mechanism behind healthy people not getting C. difficile infections?
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
Typhoid fever presentation
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
Mucus diarrhea, cauliflower-like mass in sigmoid colon indicates...
Villous adenoma

STEP Flash Cards (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions