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Review / Wrong Answers > 6/5 UWorld > Flashcards

6/5 UWorld Flashcards

1
Q

What is a Curling ulcer?

A

Gastric ulcer due to burns

Burns = fluid loss = hypovolemia = ischemia of gastric mucosa

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2
Q

What is a Cushing ulcer

A

Gastric ulcer due to brain injury

Brain injury = increased vagal stimulation = increased ACh = increased H+ production

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3
Q

What is Menetrier disease

A
  • Gastric hyperplasia of mucosa cells of the stomach
    • Leads to hypertrophied rugae which look like brain gyri
  • Atrophy of parietal cells = decreased gastric acid production
  • Increased risk of gastric carcinoma
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4
Q

What is Sister Mary Joseph nodule

A

Metastasis of gastric carcinoma to subcutaneous periumbilical area

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5
Q

What presents with a “double bubble” sign in the abd region on X-ray

A

Duodenal atresia

  • Failure of the duodenum to recanalize, so it is basically a blind pouch à dilation of stomach and proximal duodenum
  • Presents as bilious vomiting and abdominal distension
  • X-ray will should “double bubble”
    • Buildup of air distal to the pyloric sphincter (within the blind pouch)
    • Buildup of air proximal to the pyloric sphincter within the stomach
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6
Q

Where is secretin produced and what is its function?

A

Produced by S cells of the duodenum

Increase pancreatic HCO3- secretion in order to neutralize gastric acid

Decreases gastric acid secretion

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7
Q

Where is CCK produced and what is its function?

A

Produced by I cells of the duodenum

Stimulated in response to fatty acids

Increases pancreatic secretions

Increased gallbladder contractility

Relaxes the Sphincter of Oddi

Decreases gastric emptying

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8
Q

Where is somatostatin produced and what is its function

A
  • Produce by D cells of pancreas and GI mucosa
  • Shuts down everything:
    • Gastrin, CCK, Secretin, GIP, VIP, Insulin, Glucagon
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9
Q

Where is VIP produced and what is its function

A
  • Relaxes smooth muscle and sphincters throughout the GI tract
    • Causes copious diarrhea
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10
Q

What are the retroperitoneal structures

A

o SAD PUCKER

§ S à Suprarenal (adrenal gland)

§ A à Aorta and IVC

§ D à Duodenum (2nd through 4th parts)

§ P à Pancreas (except tail)

§ U à Ureters

§ C à Colon (descending and ascending)

§ K à Kidneys

§ E à Esophagus (thoracic portion)

§ R à Rectum (partially)

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11
Q

Presentation of tropical sprue

A
  • Unknown cause – probably infectious
  • Looks like celiac but:
    • Affects the entire small bowel
      • Vs. Celiac which mainly affects distal duodenum and proximal jejunum
    • Responds to antibiotics
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12
Q

What disease is associated with anti-transglutaminase

A

Celiac disease

Also associated with anti-gliadin

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13
Q

What disease is assocaited with weight loss, lymphadenopathy, hyperpigmentation, cardiac symptoms, arthralgias, neurologic symptoms

A

Whipple disease

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14
Q

Describe Whipple disease (cause, symptoms, histology)

A

Infection with Tropheryma whipplei

Symptoms:

Weight loss, lymphadenopathy, hyperpigmentation, cardiac symptoms, arthralgias, neurologic symptoms

Histology:

PAS (+) foamy macrophages in intestinal lamina propria

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15
Q

What is the characteristic histology of abetalipoproteinemia

A
  • Will see abnormal star-shaped RBCs called acanthocytes (spur cells) - irregular spikes (vs. Echinocytes/burr cells)
  • Lack of apoprotein B
    • B48 needed for chylomicron secretion from the intestinal cells
      • Enterocytes fill with chylomicrons that cannot pass into circulation
      • Fat malabsorption, steatorrhea, failure to thrive
    • B100 needed for LDL reuptake in the liver
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16
Q

What is boerhaave syndrome

A
  • Transmural, usually distal esophageal rupture
  • Due to violent retching
  • Surgical emergency
17
Q

What organelle is the primary site of ribosome synthesis?

A

Nucleolus

18
Q

What immune cells are involved in the formation of caseating granulomas in TB?

A

CD4+ Th1 cells and macrophages

19
Q

Is gout or pseudogout more likely to be associated with myeloproliferative disorders

A

Gout

Myeloproliferative disorders = increased cell turnover = increased uric acid

20
Q

What is the cause and effect of sorbitol accumulation in diabetes?

A
  • Recall:
    • Glucose –> (aldose reductase) –> sorbitol –> (sorbitol dehydrogenase) –> fructose
  • Sorbitol accumulation in organs with aldose reductase and decreased or absent sorbitol dehydrogenase
  • Sorbitol is an osmol that increases osmotic pressure leading to osmotic damage, causing:
    • Neuropathy (glove and stocking)
    • Retinopathy
    • Cataracts
    • Nephropathy
21
Q

What is the enzyme that converts glucose to sorbitol?

Sorbitol to fructose?

A

Glucose –> (aldose reductase) –> Sorbitol

Sorbitol –> (sorbitol dehydrogenase) –> Fructose

22
Q

Which hormones use the cAMP pathway (Gs and Gi)

A
  • Most hormones of anterior pituitary
  • FSH, LH, ACTH, TSH, hCG, MSH, GHRH, CRH, PTH, calcitonin, glucagon, V2 vasopressin receptor
  • THINK: FLAT ChAMP
    • FSH, LH, ACTH, TSH, CRH and calcitonin, hCG, ADH (V2), MSH, PTH
23
Q

Which hormones use the IP3 pathway (Gq)

A
  • Hormones of posterior pituitary minus V2
  • GnRH, TRH, oxytocin, V1 vasopressin receptor, H1 histamine receptor, angiotensin II, gastrin
  • THINK: GOAT HAG
    • GnRH, Oxytocin, ADH (V1), TRH, Histamine (H1), Angiotensin II, Gastrin
24
Q

Which hormones use the cGMP pathway?

A
  • Vasodilators
  • Nitric oxide (NO), Atrial natriuretic peptide (ANP)
25
Q

Which hormones use steroid receptors?

A
  • Estrogens, progesterone, testosterone, glucocorticoids, aldosterone, thyroid hormone (T3/T4), vitamin D
  • THINK: VETTT CAP
    • Vitamin D, Estrogen, Testosterone, T3, T4, Cortisol, Aldosterone, Progesterone
26
Q

Which hormones use tyrosine kinase receptors?

A
  • Insulin, insulin-like growth factor (IGF-1), platelet derived growth factor (PDGF), fibroblast growth factor (FGF)
  • THINK: insulin + all the –GF’s
27
Q

Which hormones use nonreceptor tyrosine kinase (JAK/STAT)

A
  • Prolactin, cytokines (IL-2, IL-6, IFN), GH, G-CSF, Erythropoietin, Thrombopoeitin
  • THINK: PIGGLET
    • Prolactin, Immunomodulators (cytokines, IL-2, IFN), Growth hormone, Granulocyte colony stimulating factor, (No L), EPO, Thrombopoietin
28
Q

What bug stains with aniline dye?

A

Diptheria

  • Metachromatic granules will stain red and the rest of the cell will stain blue
29
Q

What is the MOA of diptheria toxin

A

AB exotoxin inhibits protein synthesis by ADP-ribosylation of elongation factor (EF) 2

30
Q

What part of the pancreas forms from the ventral vs. dorsal bud?

A
  • Ventral bud:
    • Form the uncinated process, a portion of the pancreatic head, and the proximal portion of the main pancreatic duct
  • Dorsal bud:
    • Forms pancreatic tail, body, most of the head, and the small accessory pancreatic duct
  • Pancreas divisum
    • Ventral and dorsal parts fail to fuse
    • Dominant dorsal duct opens into the duodenum via the major papilla and is responsible for draining the majority of the pancreas
    • Smaller ventral duct opens into the major papilla and drains the inferior/posterior head and uncinated process
31
Q

what is the main cause of death via opioid overdose

A

respiratory depression

32
Q

What are the possible karyotypes of a partial mole

A

69, XXX (1 X from egg and 2 X from sperm)

69, XXY (1 X from egg, 1 X from sperm, 1 Y from sperm)

69, XYY (1 X from egg, 2 Y from sperm)

33
Q

What are the possible karyotypes of a complete mole?

A
  • Empty ovum fertilized by sperm – 46 chromosomes
    • (90% of cases) Can be fertilized by one sperm which then duplicates
      • 46, XX
        • 46, YY zygote would not survive
    • Can be fertilized by two sperm
      • 46, XX or 46, XY
34
Q

What is the drug Baclofen used fo

A
  • GABA-B receptor agonist
  • Treats spasticity secondary to both brain and spinal cord disease, including multiple sclerosis
35
Q

What other symptoms (besides proximal muscle weakness) are often seen in Lambert-Eaton?

A
  • Autonomic symptoms (dry mouth, impotence)
36
Q

What is the pathogenesis of thrombotic thrombocytopenic purpura (TTP)

A
  • Platelets used up in pathologic formation of microthrombi in small vessels
  • Due to decreased ADAMTS13, enzyme that normally cleaves vWF for degradation
    • No vWF degradation = abnormal platelet adhesion = microthrombi
37
Q

What is the pathogenesis behind immune thrombocytopenia (ITP)

A
  • IgG autoantibodies to GP2b3a
  • Antibodies produced by plasma cells of spleen and antibody-bound platelets consumed by macrophages of spleen
38
Q

What is the defect in Bernard-Soulier syndrome

A
  • Defect of glycoprotein 1b
  • Platelet can’t bind to vWF on collagen = defect of platelet plug formation
  • Platelet count is only slightly low – moderate thrombocytopenia
  • Large platelets
39
Q

What is the defect in Glanzmann thrombasthenia

A
  • Genetic GP2b3a deficiency
  • Defect in platelet aggregation
  • Platelet count is normal (they aren’t being destroyed, just can’t aggregate)

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