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ComBANK Review > Week #1 > Flashcards

Week #1 Flashcards

1
Q

What is the function of the choroid plexus?

A

CSF production

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2
Q

What is a choroid plexus papilloma (CPP)?

A

Benign neoplasm of the choroid plexus villi

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3
Q

What age is most commonly affect by CPPs?

A

Children less than 2 y/o

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4
Q

What are the major clinical manifestations of a CPP?

A

Hydrocephalus

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5
Q

What neuroanatomical structure lies just inferior to the 3rd ventricle?

A

Hypothalamus

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6
Q

What hypothalamic nucleus is responsible for satiety?

A

Ventromedial nucleus (VMN)

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7
Q

What is the clinical manifestations of damage to VMN e.g. in a CPP putting pressure in the VMN of the hypothalamus?

A

Hyperphagia and weight gain

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8
Q

In Bell Palsy, is the effected facial nerve/ facial nerve nucleus on the ipsilateral or contralateral side?

A

Ipsilateral

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9
Q

Where is the nucleus of the facial nerve located?

A

The rule of four: there are 4 cranial nerves in the medulla, 4 in the pons and 4 above the pons (2 in the midbrain)

Medulla= 9-12 
Pons= 5-8 
Midbrain= 3 and 4
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10
Q

Are the CN VII nuclei located medially or laterally? What is the mnemonic to remember?

A

Nucleus is located laterally

  • Odd motor nuclei do NOT divide equally into 12
  • 4 motor nuclei that are in the midline are those that divide equally into 12 except for 1 and 2, that is 3, 4, 6 and 12
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11
Q

What is the defect seen in Von Willebrand Disease?

A

Autosomal dominant defect in vWF

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12
Q

What is the normal role of vWF in clotting?

A
  • vWF is released from storage granules in platelets and endothelial cells. It performs two major roles:
    1) mediates the adhesion of platelets to sites of vascular injury
    2) binds and stabilizes the procoagulant protein factor VIII
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13
Q

What are the expected Bleeding Time (BT), PT, and PTT in Von Willebrand Disease?

A
  • BT is increased
  • PT is normal
  • PTT may be increased or normal
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14
Q

What clinical scenario should make you suspicious for von Willebrand Disease?

A

Young woman with menorrhagia (heavy menses) and a family history of the same (autosomal dominant)

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15
Q

What is the MOA of ADH? Where does ADH exert its mechanism of action?

A

ADH increases the insertion of aquaporins into principal cells of the collecting tubule in the nephron

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16
Q

What type of lung cancer is SIADH associated with?

A

Small cell lung cancer

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17
Q

What is the MOA of Acetazolamide?

A

Carbonic anhydrase inhibitor

- Causes “self-limited” NaHCO3 diuresis and decreases total body HCO3-

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18
Q

What are the clinical indications for Acetazolamide?

A

1) Glaucoma
2) Urinary alkalinization
3) Metabolic acidosis
4) Altitude sickness
5) Pseudotumor cerebri

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19
Q

What adverse effects are associated with Acetazolamide?

A

1) Hyperchloremic metabolic acidosis
2) Paresthesias
3) NH3 toxicity
4) Sulfa allergy

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20
Q

What is an alternative name for Adhesive Capsulitis?

A

Frozen Shoulder Syndrome

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21
Q

What is Adhesive Capsulitis?

A

Progressive pain and restriction of the should that worsens over the course of a year

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22
Q

What is the typical etiology of Adhesive Capsulitis?

A

Prolonged immobility of the shoulder

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23
Q

Oxytocin is secreted by what gland? Where is Oxytocin synthesized?

A

Oxytocin is secreted by the posterior pituitary; however, it is synthesized in the hypothalamus

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24
Q

What specific nucleus of the hypothalamus makes oxytocin?

A

Paraventricular

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25
Q

What is the steroidal precursor to estrogen?

A

Androstenedione

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26
Q

What artery is implicated in lateral medullary infarctions? What is the resulting syndrome called?

A

Posterior Inferior Cerebellar Artery (PICA)

*Infarction is called “Lateral Medullary Syndrome”

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27
Q

What structures receive blood supply from the PICA?

A

1) Vestibular nuclei
2) Lateral spinothalamic tract- pain and temperature
3) Spinal trigeminal nucleus
4) Nucleus ambiguus
5) SNS fibers
6) Inferior cerebellar peduncle

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28
Q

What are the symptoms of a PICA infarction?

A

1) Vomiting
2) Vertigo
3) Nystagmus (horizontal)–TOWARD lesion
4) Decreased pain and temperature sensation from the ipsilateral face and contralateral body
5) DYSPHAGIA
6) HOARSENESS
7) Decreased gag reflex
8) Ipsilateral horner’s syndrome

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29
Q

What spinal tract carries pain and temperature sensation?

A

Spinothalamic

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30
Q

Describe the typical presentation of sensory findings in Lateral Medullary Syndrome.

A
  • Loss of pain and temperature to the ipsilateral face

- Loss of pain and temperature to the contralateral body

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31
Q

What is Autosomal Dominant Polycystic Kidney Disease (ADPKD)?

A
  • Adult form of polycystic kidney disease
  • Numerous cysts cause bilaterally enlarged kidneys
  • Destroys kidney parenchyma
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32
Q

What is the typical presentation of ADPKD?

A

1) Flank pain
2) Hematuria
3) HTN
4) Urinary infection
5) Progressively renal failure

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33
Q

What can cause acute flank pain is ADPKD?

A

Cyst rupture

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34
Q

What is the genetic basis for ADPKD?

A

Autosomal Dominant mutation in:

  • PKD1 on chromosome 16*
  • PKD2 on chromosome 4
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35
Q

What is ADPKD associated with?

A

1) Berry aneurysm*
2) MVP
3) Benign hepatic cysts

*Also called a saccular aneurysm, this is a round outpouching of the cerebral arteries

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36
Q

What age is ARPKD seen in?

A

This is the childhood form of PKD

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37
Q

Where do Saccular (berry) aneurysms occur?

A

Bifurcations in the Circle of Willis

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38
Q

What is the most dreaded complication of a Saccular Aneurysm?

A

Rupture

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39
Q

When a Saccular Aneurysm ruptures, what is the typical result?

A

Subarachnoid hemorrhage (SAH)

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40
Q

How do patient’s typical present with a SAH?

A

“Worst headache of my life”

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41
Q

What are the functions of the dorsal and palmar interossei muscles of the hand? What is the mnemonic to remember?

A

DAB and PAD

Dorsal interossei ABduct
Palmar interossei ADduct

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42
Q

What is endometrial hyperplasia?

A

Abnromal endometrial gland proliferation

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43
Q

What usually causes endometrial hyperplasia?

A

Excess estrogen stimulation

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44
Q

How does endometrial hyperplasia present?

A

Postmenopausal vaginal bleeding

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45
Q

What are the risk factors for endometrial hyperplasia?

A

1) Anovulatory cycles
2) Hormone replacement therapy
3) PCOS
4) Granulosa cell tumor

Also, late menopause, nulliparity, and obesity–these factors increase the risk of unopposed estrogen

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46
Q

What does endometrial hyperplasia increase the risk for?

A

Endometrial carcinoma

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47
Q

What is the first line drug therapy for ankylosing spondylitis?

A

NSAIDs and specifically Indomethicin

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48
Q

What is the MOA of Cyclosporin?

A
  • Calcineurin inhibitor that binds to CYCLOphilin

- This prevents IL-2 transcription

49
Q

What is the other calcineurin inhibitor with a similar MOA to cyclosporine?

A

Tacrolimus (FK506)

50
Q

What are the indications for both cyclosporine and tacrolimus?

A

Transplant rejection prophylaxis

51
Q

What are the additional indications for cyclosporine compared to tacrolimus?

A

1) Psoriasis

2) RA

52
Q

What is the classic toxicity associated with the calcineurin inhibitors?

A

Nephrotoxicity

53
Q

What two adverse effects are seen with cyclosporine and NOT with tacrolimus?

A

1) Gingival hyperplasia

2) Hirsutism

54
Q

Beyond nephrotoxicity, gingival hyperplasia, and hirsutism, what are the other adverse effects associated with cyclosporine?

A

1) HTN
2) Hyperlipidemia
3) Neurotoxicity

55
Q

There are three major esophageal pathologies that are emergencies associated with alcoholics, what are they?

A

1) Ruptured esophageal varice
2) Mallory-Weiss Syndrome
3) Boerhaave Syndrome

56
Q

What distinguishes Mallory-Weiss Syndrome from Boerhaave Syndrome?

A

Mallory-Weiss Syndrome= lacerations of the distal esophagus from violent retching

Boerhaave Syndrome= transmural esophageal rupture of the distal esophagus

57
Q

What is the result of esophageal rupture in Boerhaave Syndrome, and what is the eponym for the physical exam finding that is expected?

A

Pneumomediastinum= air in the mediastinum

  • Results in a Hamman crunch
  • Hamman crunch= crackling sound with each heartbeat
58
Q

What is angiodysplasia?

A
  • This is the most common vascular anomaly of the GI tract; it results in PAINLESS hematochezia
  • Characterized by tortuous dilation of blood vessels
59
Q

What is tuberous sclerosis?

A

Neurocutaneous disorder characterized by numerous benign hamartomas

*Note that it affects nearly every organ system

60
Q

What is the inheritance pattern of tuberous sclerosis?

A

Autosomal dominant

61
Q

What is the hallmark cutaneous manifestation of tuberous sclerosis?

A

“Adenoma sebaceum” i.e. angiofibromas (cutaneous hamartomas) resulting in flat/ reddish macular lesions on the face that are first mistaken for freckles

62
Q

What tumors are associated with tuberous sclerosis?

A

1) Giant cell astrocytomas
2) Renal angiomyolipomas
3) Cardiac rhabdomyomas

63
Q

What is the most frequent primary cardiac tumor in children?

A

Rhabdomyoma

64
Q

What is agoraphobia?

A

Exaggerated fear of being in open or enclosed placing esp. including:

1) Public transportation
2) Crowds/lines
3) Leaving home alone

65
Q

What are the treatment options for agoraphobia?

A

1) CBT
2) SSRI
3) MAOI

66
Q

What class of anti-anxiety drugs is best for PRN/ short-acting use?

A

Benzodiazepines

67
Q

What is the specific mechanism of action of Benzodiazepines?

A

Enhance GABA

68
Q

Describe the pathophysiology of Achalasia.

A
  • Failure of relaxation in the LES due to loss of the Myenteric Plexus
  • Myenteric plexus produces NITRIC OXIDE SYNTHASE
  • Increases NO and causes smooth muscle relaxation of the LES
69
Q

What is the pathognomonic finding on barium swallow study in Achalasia?

A

“Birds beak”

70
Q

What is the etiology of Achalasia?

A
  • Primary is autoimmune, but poorly understood

- Secondary is from Chagas Disease or malignancy

71
Q

What is the organism that causes Chagas Disease?

A

T. cruzi

72
Q

What is the mnemonic to remember the levels of disease prevention?

A

PST

Primary= prevention 
Secondary= screening 
Tertiary= treatment
73
Q

What is the Karyotype in Turner’s Syndrome?

A

45, XO

74
Q

What are the classic clinical manifestations of Turner’s Syndrome?

A

1) Short stature
2) Ovarian dysgenesis
3) Shield chest
4) Preductal coarctation
5) Webbed neck
6) Horseshoe kidney

75
Q

Intention tremors are indicative of _____?

A

Cerebellum dysfunction

76
Q

What organism is the most likely causes of osteomyelitis in a patient with Sickle Cell anemia?

A

Salmonella and Staphylococcus aureus

77
Q

What is the most appropriate initial antibiotic therapy for a Sickle Cell patient with osteomyelitis? What antibiotics are used for the two most likely pathogens?

A

1) Ciprofloaxacin - Salmonella

2) Vancomycin - S. aureus, including MRSA

78
Q

What are the clinical indications for ECT?

A

1) Treatment refractory depression
2) Depression with psychosis
3) Suicidal ideation

79
Q

What are the adverse effects associated with ECT?

A

1) Disorientation
2) Temporal headache*
3) Anterograde and retrograde amnesia

*Most common

80
Q

What genetic mutation is associated with MEN 2A? What is the inheritance pattern for this mutation?

A

RET (neural crest cells); autosomal dominant

81
Q

What are the three clinical manifestations of MEN 2A?

A

1) Pheochromocytoma
2) Parathyroid tumor
3) Meduallary thyroid carcinoma

82
Q

What tumor marker is used to evaluate medullary thyroid carcinoma?

A

Calcitonin; serum levels correlate with tumor mass

83
Q

What is the eponym for the test that is associated with TOS caused by compression of the NVB between the anterior and middle scalenes?

A

Adson’s Test

84
Q

Describe the Adson’s Test.

A
  • Patient’s pulse is monitored on the affected side
  • Extend: elbow and arm
  • Externally rotate wrist
  • Turn head toward affected arm

*Ask the patient to take a deep breath; if pulse diminishes or is absent, test is positive

85
Q

What paraneoplastic syndrome is associated with Squamous Cell Carcinoma of the lung?

A

Hypercalcemia produced by PTHrP

86
Q

What are the expected histologic findings in squamous cell carcinoma of the lung?

A
  • Keratin pearls

- Intercellular bridges

87
Q

What is the mnemonic to remember the etiology of Duchenne Muscular Dystrophy?

A

Duchene= Deleted Dystrophin

88
Q

What is the genetic basis of DMD?

A

X-linked frameshift mutation leading to a truncated dystrophin protein

89
Q

What is the normal function of dystrophin?

A

Anchors muscle fibers in skeletal and cardiac muscle

90
Q

What is the classic presentation of DMD?

A
  • Onset prior to 5 y/o
  • Weakness of the pelvic girdle that ascends superiorly
  • Waddling gait
  • Gower maneuver
91
Q

What is the most common cause of death in DMD?

A

Dilated cardiomyopathy

92
Q

What is progressive multifocal leukoencephalopathy (PML)?

A

Demyelination of the CNS due to destruction of oligodendrocytes

93
Q

What is PML associated with?

A

JC virus infection and AIDS patients

94
Q

What bones form pterion?

A

1) Frontal
2) Temporal
3) Parietal
4) Sphenoid

95
Q

What is the purpose of the cranial V-spread technique?

A

Separation of restricted or impacted cranial sutures

96
Q

What is the MOA of Metformin?

A

Unknown but increases insulin sensitivity

*A “biguanide”

97
Q

What is the clinical indication for Metformin?

A

First-line therapy for DM-II

98
Q

What is the most serious adverse effect associated with Metformin?

A

Lactic acidosis

99
Q

When is Metformin contraindicated?

A

Renal insufficiency b/c it causes lactic acidosis

100
Q

What is the most common adverse effect associated with Metformin?

A

GI upset

101
Q

What are the first generation sulfonylureas?

A

1) Chlorpropamide

2) Tolbutamide

102
Q

What is the MOA of the sulfonylureas?

A

1) Inhibition of the K+ channel in pancreatic Beta-cells
2) Cell membrane depolarization occurs
3) Ca++ rushes in
4) Insulin is released

103
Q

Are sulfonylureas used in DM-I or DM-II?

A

DM-I; require functioning beta-cells

104
Q

What are the adverse effects associated with first and second generation sulfonylureas?

A

1st generation= disulfram-like effect

2nd generation= hypoglycemia

105
Q

What adverse effects are associated with the Ciltaones/thiazolindinediones (TZDs)?

A

1) Weight gain
2) Edema
3) Hepatotoxicity
4) HF
5) Increased risk of fracture

106
Q

What organism is associated with primary amebic encephalitis?

A

Naegleria fowleri

107
Q

What is the anterior Chapman point associated with the appendix?

A

Tip of the right 12th rib

108
Q

What is the posterior Chapman point associated with the appendix?

A

Transverse process of T11

109
Q

What are the clinical manifestations of Neurofibromatosis Type 1?

A

1) Cafe-au-lait spots
2) Cutaneous neurofibromas (proliferation of peripheral nerves)
3) Optic gliomas
4) Pheochromcytomas
5) Lisch nodules (pigmented iris hamartomas)

110
Q

What is the genetic basis for NF1?

A
  • Autosomal dominant mutations in NF1 gene
  • Chromosome 17*

Note that NF1 is also called “von Rcklinghausen” disease, which has 17 letters in the name

111
Q

What is reactive or secondary thrombocytosis?

A

Increased circulating platelets due to:

1) Malignancy
2) Trauma
3) Infection
4) S/p splenectomy
5) Iron deficiency anemia
6) Idiopathic causes

112
Q

If a joint aspiration is done in an acute gout attack, what are the expected results? How does this differ from pseudogout?

A

Aspiration with show needle shaped crystals; however,

  • Gout= NEGATIVE birefingence
  • Pseudogout= POSTIVE birefringence
113
Q

What are tophi?

A

Chalky white uric acid deposits under skin

114
Q

What are the four major attachements of the dura to the spinal column?

A

1) Foramen magnum
2) C2
3) C3
4) S2

115
Q

What ligament is the demarcation point between an upper and lower GI bleed?

A

Ligament of Treitz

116
Q

What spinal cord levels are associated with sympathetic innervation to the upper GI tract?

A

T5-T9

117
Q

What is “Chadwick’s Sign?”

A

Bluish vaginal mucosa; an early sign of pregnancy

118
Q

What is an absolute contraindication to Warfarin therapy?

A

Pregnancy b/c it is a known teratogen

ComBANK Review (2 decks)

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