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Review / Wrong Answers > 6/7 UWorld > Flashcards

6/7 UWorld Flashcards

1
Q

What structure is cut during a midline episiotomy

A

Perineal body

Midline episiotomy is a vertical incision from the posterior vaginal opening to the perineal body

Itr transects the vaginal submucosal tissue but not the external anal sphincter or the rectal mucosa

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2
Q

Describe the pathogenesis of Zenker diverticulum

A
  • Thought to be due to abnormal spasm or diminished relaxation of pharyngeal muscles during swallowing
  • Increased oropharyngeal intraluminal pressure eventually results in herniation of the pharyngeal mucosa through a zone of muscle weakness (false diverticulum) in the posterior hypopharynx
  • Pulmonary aspiration of diverticular contents may lead to recurrent pneumonia
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3
Q

What causes differentiation of Th0 cells into Th1 cells

What is produced by Th1 cells

What inhibits differentation of Th1 cells

A
  • Th1 cells
    • Differentiation caused by IL-12 (secreted by macrophages)
    • Produces IL-2 and IFN-y
    • Inhibited by IL-10
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4
Q

What causes differentiation of Th0 cells into Th2 cells

What is produced by Th2 cells

What inhibits differentiation of Th2 cells

A
  • Th2 cells
    • Differentation caused by IL-4
    • Produces IL-4, IL-5, IL-10
    • Inhibited by IFN-y
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5
Q

The most common mutation of CFTR gene causes a defect in what process?

A
  • Most common mutation (deltaF508) causes impaired post-translational processing of CFTR, which is detected by the ER, causing the abnormal protein to be targeted for proteasomal degradation, preventing it from reaching the cell surface
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6
Q

What is the presentation of a lesion to the dominant parietal cortex

A
  • Gerstmann syndrome
    • agraphia (inability to write)
    • acalculia (inability to calculate)
    • finger agnosia (inability to distinguish fingers)
    • left-right disorientation
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7
Q

What is the treatment for organophosphate poisoning

A

Organophosphates are cholinesterase inhibitors found in pesticide = increased ACh

Treatment:

  • Atropine
    • Competitively binds ACh receptors
  • Pralidoxime
    • Sketchy = lid on toxic spray
    • Regenerates acetylcholine esterase
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8
Q

What receptor does Clonidine work on

A

a1 agonist

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9
Q

Describe the receptors that dopamine acts on

A

D-B-A order of activation

Low doses of DA = DA receptors

Medium doses = Beta receptors

High doses = Alpha receptors

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10
Q

What receptors does Epinephrinw work on

A

Beta > alpha agoinst

Predominantly beta at low doses

More alpha at higher doses

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11
Q

What is the drug of choice for anaphylaxis

A

Epinephrine

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12
Q

What is the drug of choice for septic shock

A

Norepinephrine

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13
Q

What are the 2 main clinical uses of selective alpha-1 antagonists

A

HTN

BPH

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14
Q

What is the MOA of Acebutolol and Pindolol

A

Sketchy:

  • Agonizing plastic bugle
  • Agonizing pin

MOA: are partial beta-agonists, but funciton as beta blockers because their action on beta receptors is so low, and still prevents the binding of ligands that would strongly activate these receptors

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15
Q

What are the 2 drugs that act as beta-blockers and alpha-1 antagonists

A

Carvedilol (used in chronic heart failure)

Labetolol (used in HTN in pregnancy, hypertensive emergency, acute aortic dissection)

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16
Q

What is receptor does alpha-methydopa effect?

A

Alpha-2 agonist and analog of L-DOPA

Used to treat gestational HTN

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17
Q

Describe the steps of catecholamine synthesis (from phenylalanine to norepinephrine), including enzymes

A
18
Q

What are the layers of the glomerular filtration barrier and which layer is responsible for size/charge?

A
  • Fenestrated capillary endothelium
    • Size barrier
  • Basement membrane
    • Negatively charged (contains heparin sulfate) and size barrier
  • Podocyte foot process
    • Visceral layer of Bowman’s capsule
    • Negative charge layer
19
Q

Describe the fluid composition/compartements of the body

A
  • 60-40-20 rule
  • 60% of body mass is water, of that 60%:
    • 40% is ICF
    • 20% is ECF
      • Only 25% of ECF is plasma
20
Q

What substance is used to measure renal plasma flow

A
  • Renal plasma flow
    • RPF = Blood going to the glomeruli + blood going to the tubules
    • Can be estimated with PAH (Clearance of PAH > GFR)
21
Q

When does glucose begin to appear in the urine

A
  • Glucose is completely reabsorbed up until plasma glucose level ~200 mg/dL
    • This is when glucosuria begins (threshold)
  • At ~375 mg/min, all transporters are fully saturated
22
Q

Describe the rates of absorption in the proximal tubule of:

Na+, Cl-, K+, HCO3-, Urea, Glucose, Inulin, amino acids, creatinine, and PAH

Be able to graph these on a Tubular fluid / plasma filtrate graph (specifically is HCO3- more reabsorbed or secreted?)

A
  • Anything that falls below the horizontal line (1.0) – more of that soluble is being absorbed relative to water
  • Anything that falls below the horizontal line – less of that solute is being absorbed relative to water
    • The reason that Creatinine and Inulin levels within the tubule are rising is because they are not reabsorbed, but water is, so their relative levels go up
    • PAH is not being reabsorbed and is also being secreted into the tubules
  • Interpretation of graph:
    • PAH is freely filtered and secreted
    • Creatinine is also freely filtered but not secreted as much as PAH
    • Inulin is freely filtered but not secreted or reabsorbed
      • Clearance of Inulin = GFR
    • Urea is freely filtered and poorly reabsorbed
    • Na+ and K+ are reabsorbed at the same rate of water so their concentrations remain constant
    • HCO3- is actively reabsorbed due to carbonic anhydrase
    • Glucose and amino acids are almost 100% reabsorbed in the proximal tubule
23
Q

What part of the nephron are divalent cations (Mg2+ and Ca2+) reabsorbed and how?

A

Thick ascending loop

  • Indirectly induces reabsorption of Mg2+ and Ca2+
    • K+ enters the cell from the lumen via NKCC but then leaks back into the lumen, giving the lumen a slight positive charge
    • Cations flow from lumen into cell down the electric gradient
24
Q

Describe how you get euvolemic hyponatremia in SIADH

A

Increased ADH leads to excessive water retention

Body responds to water retention with decreased renin and aldosterone, increased ANP and BNP

Causes increase urinary Na+ secretion - Euvolemic hyponatremia

25
Q

Describe the defect in type 1 renal tubular acidosis, hyper/hypokalemia, urine pH

A
  • Distal renal tubular acidosis à defect in collecting tubule
  • Alpha-intercalated cells are unable to secrete H+ à acidosis
  • Hypokalemia
  • Urine pH will be > 5.5 (because no H+ in urine)
  • THINK:
    • Type 1 = impaired H+ excretion = H is 1 letter
26
Q

Describe the defect in type 2 renal tubular acidosis, hyper/hypokalemia, urine pH

A
  • Proximal renal tubular acidosis à defect in proximal tubule
  • Impaired HCO3- reabsorption à acidosis
  • Hypokalemia and hypophosphatemia
  • Urine pH < 5.5
27
Q

Describe the defect in type 4 renal tubular acidosis, hyper/hypokalemia, urine pH

A
  • Hyperkalemic renal tubular acidosis
  • Due to hypoaldosteronism à decreased K+ secretion à hyperkalemia
  • Hyperkalemia prevents collecting tubules from generating NH4+ à impaired ammonium excretion
  • Urine pH < 5.5.
  • THINK:
    • Type 4 = impaired NH4 excretion due to aldosterone (aldo) = 4 = NH4 and Aldo is 4 letters
28
Q
A
29
Q

What is the normal value for filtration fraction (FF)

A

FF = GFR/RPF

Normal = 20%

30
Q

Causes of metabolic acidosis

A
  • Anion gap = Adding acid to the blood
    • MUDPILES:
      • M – Methanol
      • U – Uremia (renal failure)
      • D – Diabetic ketoacidosis
      • P – Propylene glycol/Paraldehyde
      • I – Isoniazid/Iron
      • L – Lactic acidosis
      • E – Ethylene glycol (antifreeze)
      • S – Salicylates (aspirin)
  • Non-anion gap = Losing excessive HCO3-
    • Diarrhea, Renal tubular acidosis, Spironolactone, Acetazolamide
31
Q

Causes of metabolic akalosis

A
  • Losing H+ = excessive vomiting, diuretics, hyperaldosteronism
32
Q

What is Winter’s fomula and what does it do?

A
  • Predicted respiratory compensation for metabolic acidosis
    • If measured pCO2 > predicted pCO2 – concomitant respiratory acidosis
    • If measure pCO2 < predicted pCO2 – concomitant respiratory alkalosis
  • pCO2 = 1.5(HCO3-) + 8 +/- 2
33
Q

Which renal tubular acidoses are associated with hypokalemia and which with hyperkalemia

A

Type 1 = hypokalemia

Type 2 = hypokalemia

Type 4 = hyperkalemia

34
Q

Which renal tubular acidoses are associated with urine pH > 5.5 vs < 5.5

A

Type 1 = > 5.5 (a-intercalated cells unable to secrete H+)

Type 2 = < 5.5 (urine is acidified by a-intercalated cells in collecting tubule)

Type 4 = < 5.5

35
Q

What is the formula for anion gap?

A

Na - (Cl + HCO3)

> 12 = anion gap

8-12 = non-anion gap

36
Q

Disease associated with anti-mitochondrial antibody

A

Primary biliary cholangitis

  • Autoimmune destruction of intra-hepatic bile ducts
    • Associated with other autoimmune conditions
  • Lymphocytic infiltrate + granulomas
37
Q

What is the cause of fixed splitting int the heart

A

ASD (L to R shunt)

38
Q

Differentiate malingering from factitious disorder

A
  • Malingering = conscious production of symptoms with conscious drive
    • Patient consciously fakes symptoms in order to obtain secondary (external) gain
  • Factitious disorder = conscious production of symptoms with unconscious drive
    • Patient consciously fakes symptoms in order to obtain primary gain (sick role)
    • Subtypes:
      • Munchausen = chronic factitious disorder with predominantly physical signs and symptoms
      • Munchausen by proxy = Illness fabricated by caregiver
39
Q

Cause of flushing in response to Niacin

A

Prostaglandins

40
Q

MOA of toxin involved in EHEC

A

Shiga-like toxin (same MOA as Shiga toxin)

  • Inactivates 60S ribosome by removing adenine from rRNA
41
Q

What do HOX genes encode for?

A

o Codes for transcription factors that will alter the expression of genes involved in the segmental organization of the embryo in craniocaudal direction

o Hox mutation = appendages in wrong location

42
Q

MOA of alpha-toxin of C. perfringens

A

Toxin is a lecithinase - degrades lecithine, a component of phospholipid membranes, leading to cell death and necrosis

Review / Wrong Answers (140 decks)

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