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Mixed 3 Flashcards

1
Q

Why do patients with Zollinger Ellison syndrome develop malabsorption?

A

Inactivation of pancreatic enzymes by increased production of stomach acid and injury to the mucosal brush border

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2
Q

2 locations of the gastrin-producing tumor in ZES?

A

Pancreas

Duodenum

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3
Q

MEN1 screening labs?

A

Parathyroid hormone
Ionized calcium
Prolactin

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4
Q

First-line pharmacotherapy for bulimia nervosa?

A

SSRIs; fluoxetine has the best evidence for reducing the frequency of bingeing and purging episodes (most effective as part of multimodal therapy - nutritional rehabilitation, CBT)

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5
Q

Clinical presentation - intense fear of gaining weight, distorted view of body weight and shape, BMI <18.5

A

Anorexia nervosa

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6
Q

Rx anorexia nervosa?

A

CBT
Nutritional rehabilitation
Olanzapine if no response

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7
Q

Clinical presentation - recurrent episodes of binge eating, lack of control during eating, no compensatory behaviors

A

Binge-eating disorder

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8
Q

Rx binge-eating disorder?

A

CBT
Behavioral weight loss therapy
SSRI
Lisdexamfetamine

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9
Q

Presentation - recurrent episodes of binge eating, excess worrying about body shape and weight, maintains normal to increased body weight, binge eating with compensatory behaviors (purge, exercise, fast, laxatives)

A

Bulimia nervosa

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10
Q

Rx bulimia nervosa?

A

CBT
Nutritional rehabilitation
SSRI (fluoxetine)

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11
Q

Lab abnormality associated with self-induced vomiting?

A

Hypokalemia

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12
Q

Why is chronic constipation a risk factor for recurrent cystitis in toddlers?

A

Impacted stool can cause rectal distention, which in turn compresses the bladder, prevents complete voiding, and leads to urinary stasis

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13
Q

Risk factors for pediatric constipation?

A

Initiation of solid food and cow’s milk
Toilet training
School entry

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14
Q

Clinical features of pediatric constipation?

A

Painful/hard bowel movements
Stool withholding
Encopresis

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15
Q

Complications of pediatric constipation?

A

Anal fissures
Hemorrhoids
Enuresis/UTIs

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16
Q

Rx pediatric constipation?

A

Increased dietary fiber and water intake
Limit cow’s milk intake to <24 oz
Laxatives
+/- suppositories/enema

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17
Q

Presentation - continuous, painless, watery discharge with normal wet mount microscopy after pelvic surgery

A

Vesicovaginal fistula

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18
Q

Risk factors for vesicovaginal fistula?

A

Pelvic surgery
Pelvic irradiation
Prolonged labor/childbirth trauma
GU malignancy

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19
Q

Dx vesicovaginal fistula?

A

Physical exam (visible vaginal defect, may have visible granulation tissue)
Dye test
Cystourethroscopy

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20
Q

Presentation - vaginal discharge that is painless, thin, gray, and malodorous

A

BV

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21
Q

Dx BV?

A

Visualization of >20% of squamous epithelial cells coated with bacteria (ie clue cells) on wet mount microscopy

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22
Q

First step in managing bilious emesis in the neonate?

A

Stop feeds
NG tube decompression
IV fluids

Abdominal XR

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23
Q

List the 4 major findings of the 4 major causes of bilious emesis in the neonate on abdominal XR

A
  1. Double bubble sign (duodenal atresia)
  2. NG tube in misplaced duodenum (malrotation)
  3. Dilated loops of bowel (meconium ileus or Hirschsprung disease)
  4. Free air, hematemesis, unstable vital signs (perforation/rupture)
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24
Q

If NG tube is misplaced in the duodenum, what is the next step?

A

Upper GI series - if ligament of Treitz is on the right side of the abdomen -> malrotation

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25
Q

If dilated loops of bowel are seen on abdominal XR, what is the next step?

A

Contrast enema

If microcolon - meconium ileus
If rectosigmoid transition zone - Hirschsprung

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26
Q

Imaging should only be performed in stable neonates with bilious emesis to delineate the level of the obstruction and identify complications. What determines stability?

A

Age-appropriate vital signs, lack of hematemesis

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27
Q

Rx meconium ileus?

A

Hyperosmolar enema; surgery if unsuccesful

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28
Q

Meconium ileus is virtually pathognomonic for ___.

A

CF

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29
Q

What is the predominant mutation responsible for defective chloride transport and tenacious secretions in CF?

A

Delta F508

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30
Q

Work-up for suspected Hirschsprung disease (after noting transition zone with contrast enema)?

A

Rectal biopsy

Anorectal manometry if biopsy results are equivocal

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31
Q

Prior to prescribing SSRIs, what side effects should be discussed with patients?

A

Early side effects - headache, nausea, insomnia/sedation, anxiety, dizziness, etc.

Late side effects - sexual dysfunction, weight gain, etc.

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32
Q

AE of what medication - new-onset DM2, hepatic dysfunction, myalgia

A

Statins (HMG-CoA reductase inhibitors)

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33
Q

AE of what medication - fatigue, palpitations, peripheral edema

A

CCBs

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34
Q

AE of what medication - diarrhea, lactic acidosis, weakness

A

Metformin

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35
Q

AE of what medication - cough, dizziness, hyperkalemia

A

ACEIs

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36
Q

Most common cause of primary postpartum hemorrhage?

A

Uterine atony

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37
Q

What causes uterine atony?

A

Failure of the uterus to contract and compress the placental site blood vessels

38
Q

Presentation of uterine atony?

A

Profuse vaginal bleeding

Soft (boggy) and enlarged uterus

39
Q

Risk factors for uterine atony?

A

Prolonged labor (uterine fatigue)
Induction of labor (oxytocin receptor saturation -> unresponsive to oxytocin)
Operative vaginal delivery
Fetal weight >4000 g (8.8 LB) (over-distension of the uterus)
Hypertensive disorders

40
Q

How is hemostasis achieved after placental delivery?

A
  1. Clotting

2. Compression of the placental site blood vessels by myometrial contraction

41
Q

Initial treatment of postpartum hemorrhage 2/2 uterine atony?

A

Assess vitals, give IV fluids to maintain systolic blood pressure, transfuse appropriate blood products
Bimanual uterine massage
Uterotonic agents like oxytocin (first line)

42
Q

If oxytocin and bimanual massage fail, what is the next step in managing postpartum hemorrhage 2/2 uterine atony?

A

Administer other uterotonic agents:

  • Methylergonovine - causes smooth muscle constriction, uterine contraction, and vasoconstriction
  • Carboprost - synthetic prostaglandin that stimulates uterine contraction
43
Q

Important contraindication to use of methylergonovine?

A

History of hypertension

44
Q

Important contraindication to use of carboprost?

A

Asthma (causes bronchoconstriction)

45
Q

Stranger anxiety is a normal part of development characterized by crying when an unfamiliar person approaches. It typically peaks at age ___ and resolves by age ___.

A

8-9 months; 2 years

46
Q

If an infant does not respond to his or her name by age ___, it may represent an early sign of an autism spectrum disorder and should be followed up with further evaluation.

A

12 months

47
Q

General dx criteria of mild neurocognitive disorder?

A

Mild decline in 1+ cognitive domains

Normal functioning in all ADLs with compensation

48
Q

General dx criteria of major neurocognitive disorder?

A

Significant decline in 1+ cognitive domains
Irreversible global cognitive impairment
Marked functional impairment

49
Q

General dx criteria of Dementia with Lewy bodies?

A

Dementia + 2 or more fo the following:

  • Hallucinations
  • Parkinsonism
  • REM sleep behavior disorder
  • Fluctuations in levels of alertness
50
Q

Classic congenital adrenal hyperplasia occurs due to ___ deficiency and leads to buildup of ___ and ___. Inheritance pattern?

A

21-hydroxylase deficiency; 17-hydroxyprogsterone and testosterone; AR

51
Q

Presentation of classic congenital adrenal hyperplasia?

A

Salt-wasting syndrome in neonatal boys and girls (hypotension, dehydration, vomiting)

Ambiguous genitalia in girls (ranges from clitoromegaly to a curved, underdeveloped phallus with displaced urethral meatus; non-palpable gonads, as ovaries are intra-abdominal and testes are not present)

52
Q

Lab findings in classic congenital adrenal hyperplasia?

A

Decreased sodium
Increased potassium
Decreased glucose

53
Q

Rx classic congenital adrenal hyperplasia?

A

Glucocorticoids and mineralocorticoids
High-salt diet
Genital reconstructive surgery for girls
Psychosocial support

54
Q

What causes androgen insensitivity syndrome and how does it present?

A

Defect in the androgen receptor; presents in a genotypic male (46, xY) with undervirilized, ambiguous, or female external genitalia

55
Q

Presentation of exogenous testosterone exposure?

A

Virilization of females may occur, but 17-OHP would b enormal

56
Q

What causes placental aromatase deficiency and how does it present?

A

Prevents conversion of placental adrogens into estrogens, leading to excess virilization of the female fetus (mother is also typically virilized)

57
Q

Neonatal tetanus can occur in infants born to unimmunized mothers, frequently following ___ infection.

A

Umbilical stump

58
Q

Presentation of neonatal tetanus?

A

Difficult feeding, trismus

Spasms and hypertonicity (clenched hands, dorsiflexed feet, opisthotonus)

59
Q

Rx neonatal tetanus?

A

Supportive

ABX (penicillin) and tetanus immune globulin

60
Q

Describe the pathogenesis of tetanus.

A

C. tetani secretes tetanospasmin, which is transported retrograde to the CNS via axon. Exocytosis proteins are cleaved, inhibiting GABA and glycine release. The motor neuron is disinhibited, leading to increased muscle tone and spasms

61
Q

What are hazard ratios?

A

Ratio of an event rate occurring in the treatment group vs. the non-treatment group

62
Q

What does a hazard ratio <1 or >1 mean?

A

<1 indicate that the treatment group had a lower event rate

> 1 indicate that the treatment group had a higher event rate

63
Q

When the treatment regimen selected for a patient depends on the severity of the patient’s condition, a form of selection bios known as ___ can result.

A

Susceptibility bias (confounding by indication)

64
Q

How is selection bias avoided?

A

Patients are randomly assigned to treatments to minimize potential confounding variables

Studies may also perform an intention-to-treat analysis (compares the initial randomized treatment groups regardless of the eventual treatment to avoid counting crossover patients)

65
Q

What is lead-time bias?

A

2 disease interventions are compared and one diagnoses the disease earlier than the other without an effect on outcome - this makes it appear that the intervention prolonged survival when it really just diagnosed the disease sooner

66
Q

What is the most common cause of abnormal hemostasis in patients with chronic renal failure?

A

Platelet dysfunction

67
Q

Coag study results in chronic renal failure?

A

Normal aPTT, PT, thrombin time (TT)
Prolonged bleeding time
Normal platelet count

68
Q

Rx coagulopathy in uremic patients?

A

Desmopressin (DDAVP)
Cryoprecipitate
Conjugated estrogens

69
Q

MOA - DDAVP?

A

Increases release of factor 8:VWf multimers from endothelial storage sites

70
Q

Symptoms of malabsorption in general?

A

Bulky, foul-smelling, floating stools

71
Q

Symtpoms of fat and protein malabsorption?

A

Loss of muscle mass, loss of subcutaneous fat, fatigue

72
Q

Symptoms of iron malabsorption?

A

Pallor (anemia), fatigue

73
Q

Symptoms of calcium and vitamin D malabsorption?

A

Bone pain (osteomalacia), fracture (osteoporosis)

74
Q

Symptoms of Vitamin K malabsorption?

A

Easy bruising

75
Q

Symptoms of Vitamin A malabsorption?

A

Hyperkeratosis

76
Q

Dx celiac disease?

A

IgA anti-tissue transglutaminase

IgA anti-endomysial antibodies

77
Q

Many patients with biopsy-confirmed celiac disease will have negative test results on IgA antibody testing - why?

A

Selective IgA deficiency (common in celiac disease)

78
Q

If IgA serology is negative but the suspicion for celiac disease is high, what should be measured?

A

Total IgA (or IgG-based serologic testing)

79
Q

Internuclear ophthalmoplegia is a disorder of conjugate horizontal gaze that results from damage to the ___.

A

Medial longitudinal fasciculus

80
Q

Presentation of internuclear ophthalmoplegia?

A

Affected eye (ipsilateral to the lesion) is unable to adduct; contralateral eye abducts with nystagmus

Convergence and pupillary light reflex are preserved

81
Q

Cause of unilateral MLF lesions?

A

Lacunar stroke in the pontine artery distribution

82
Q

Cause of bilateral MLF lesions?

A

MS (classic)

83
Q

What is the medial longitudinal fasciculus?

A

Paired neural tract that mediates communication between CN III (oculomotor) and CN VI (abducens) nuclei, allowing for coordinated horizontal eye movements

84
Q

Lesion of the abducens nerve?

A

Lateral rectus palsy, inability to abduct eye

85
Q

Lesion in the Edinger-Westphal nucleus?

A

Ipsilateral fixed and dilated pupil that is non-reactive to light or accommodation

86
Q

Lesion in the lateral geniculate nucleus?

A

Contralateral homonymous hemianopsi (located in thalamus, relays visual information to ipsilateral primary visual cortex)

87
Q

Lesion in medial lemniscus

A

Contralateral loss of vibration, proprioception, light touch

88
Q

Lesion in oculomotor nerve?

A

Mydriasis, ptosis, and down and out deviation of ipsilateral eye

89
Q

Lesion in trochlear nerve?

A

Vertical diplopia that worsens when the affected eye looks down and towards the nose

90
Q

Thyroid lymphoma is uncommon, but the incidence is ~60x greater in patients with ___.

A

Preexisting chronic lymphocytic (Hashimoto) thyroiditis

91
Q

Presentation of thyroid lymphoma?

A

Rapidly enlarging, firm goiter associated with compressive symptoms (dysphagia, hoarseness, etc.). As with other lymphomas, patients may have systemic B symptoms.

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