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ComBANK Review > WEEK #2 > Flashcards

WEEK #2 Flashcards

1
Q

What is the first line treatment for strep throat?

A

PCN

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2
Q

What is the second line treatment for strep throat?

A

Macrolides e.g. erythromycin

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3
Q

EIEC and EHEC both present with bloody diarrhea. How can EIEC and EHEC be differentiated clinically?

A

EHEC= no fever or WBCs in stool sample

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4
Q

How can EIEC and EHEC be differentiated in the lab?

A

EHEC does NOT ferment sorbitol on MacConkey agar; EIEC does

Thus, use SORBITOL to differentiate in the lab

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5
Q

PT and PTT are associated with which arms of the coagulation cascade? How can you remember the difference?

A 
Extrinsic= less stuff in the pathway; PT 
Intrinsic= more stuff in the pathway: PTT
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6
Q

Hemophilia A results from what deficiency?

A

Deficiency of factor VIII

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7
Q

Hemophilia B results from what deficiency?

A

Deficiency of factor IX

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8
Q

Hemophilia C results from what deficiency?

A

Deficiency of factor XI

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9
Q

What are the inheritance patterns of the different Hemophilias: A, B, and C?

A

Hemophilia A= XR
Hemophilia B= XR
Hemophilia C= AR

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10
Q

What are the expected PT, PTT, and platelet count associated with Hemophilia A?

A

Increased PTT b/c Factor VIII is part of the intrinsic pathway (more stuff)

  • PT will be normal
  • Platelet count will be normal
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11
Q

What electrolyte abnormality is associated with Sarcoidosis?

A

Hypercalcemia

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12
Q

Why can patients with Sarcoidosis have hypercalcemia?

A
  • Sarcoidosis is characterized by immune-mediated non-caseating granulomas
  • Granulomas secrete 1,25-Vitamin D
  • Macrophage 1-a hydroyxlase can activate 1,25-Vitamin D to active Vitamin D
  • Increased Vitamin D causes hypercalcemia
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13
Q

What is the first-line treatment for bacterial vaginosis?

A

Metronidazole

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14
Q

Why does thiamine deficiency lead to Wernicke-Korsakoff Syndrome/ CNS impairment?

A
  • Thiamine is important for preventing accumulation of intracellular free radicals
  • Deficiency leads to accumulation of free radicals and mitochondiral dysfunction
  • This leads to OXIDATIVE DAMAGE to the CNS

Specifically, the Medial Dorsal Nucleus of the Thalamus and Mamillary Bodies

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15
Q

What type of disease is Goucher Disease?

A

Lysosomal Storage Disease

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16
Q

What is the genetic basis for Goucher Disease?

A

Autosomal recessive defect in Glucocerebrosidase

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17
Q

What product accumulates in lysosomes in Goucher Disease?

A

Glucocerebroside

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18
Q

What are the clinical manifestations of Goucher Disease?

A

1) Hepatosplenomegaly
2) Pancytopenia
3) Osteoporosis
4) Aseptic necrosis of the femur
5) Bone crises

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19
Q

What is the treatment for Goucher Disease?

A

Recombinant Glucocerebrosidase

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20
Q

What is the sphenobasilar synchondrosis (SBS)?

A

Articulation between the sphenoid and the occiput

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21
Q

What are the basic motions of the SBS?

A

Flexion and extension in a biphasic cycle

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22
Q

What kind of SD can trauma to the occiput result in?

A

Compression of the SBS

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23
Q

How is a compression of the 4th ventricle performed?

A

1) Cup the area of the 4th ventricle on the occiput

2) Encourage extension while prevented flexion

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24
Q

What is the MOA of Carbidopa?

A
  • Increased DA in the brain
  • Inhibits peripheral DOPA DECARBOXYLASE
  • This increases the bioavalibility of L-dopa in the CNS
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25
Q

What are the two classes of dopamine agonists used to treat PD?

A

1) Ergot
2) Non-ergot*

*Preferred

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26
Q

What is the Ergot DA agonist used to treat PD?

A

Bromocriptine

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27
Q

What are the Non-ergot DA agonists used to treat PD?

A

1) PRAMIPEXOLE

2) Ropinirole

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28
Q

What PD drugs prevent peripheral L-DOPA degradation by inhibiting COMT?

A

1) Entacapone

2) Tolcapone

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29
Q

What is Polycythemia Vera?

A

Disorder of increased RBC mass (w/ increased WBC and platelets)

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30
Q

What genetic mutation is associated with PV?

A

JAK2

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31
Q

What are the classic symptoms of PV?

A

1) Itching after a shower
2) “Erythromelalgia” i.e. severe burning-pain and red-blue discoloration due to episodic clotting of lower extremity blood vessels

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32
Q

What is Essential Thrombocytosis?

A

Disorder of increased platelets

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33
Q

What are the clinical manifestations of Essential Thrombocytosis?

A

1) Bleeding

2) Thrombosis

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34
Q

What is the characteristic finding on bone marrow biopsy of a patient with Essential Thrombocytosis?

A

Enlarged megakaryocytes

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35
Q

How will the labs of a patient with PV differ from Essential Thrombocytosis?

A 
PV= increased RBC, WBC, and platelets 
ET= Increased platelets
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36
Q

Where is the insertion of the supraspinatus muscle?

A

Greater tubercle of the humerus

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37
Q

What is Whipple Disease?

A

Bacterial infection with Treponema whipplei causing a malabsorption syndrome

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38
Q

What finding is pathognomonic for Whipple Disease?

A

PAS positive foamy macrophages in the intestinal lamina propria

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39
Q

What are the clinical manifestations of Whipple Disease?

A

Malabsorption syndrome PLUS:

1) Cardiac symptoms
2) Arthralgias
3) Neurologic symptoms

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40
Q

What is the MOA of the thiazide diuretics?

A

Inhibition of Na+/Cl- reabsorption in the Distal Convoluted Tubule (DCT)

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41
Q

What is the effect of the thiazide diuretics on Ca++?

A

Decreased Ca++ excretion

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42
Q

What is the mnemonic to remember the various side effects associated with the thiazide diuretics?

A

HyperGLUC

  • Hyperglycemia
  • Hyperlipidemia
  • Hyperuricemia
  • Hypercalcemia

Also, HYPOkalemic metabolic alkalosis and hyponatremia

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43
Q

What is the MOA of the loop diuretics?

A

Inhibition of the Na+/K+/2Cl- cotransport system in the thick ascending loop of Henle

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44
Q

What is the mnemonic to remember what happens to Ca++ with the loop diuretics?

A

“Loops lose Ca++”

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45
Q

What is the MOA of acetazolamide?

A

Carbonic anhydrase inhibitor

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46
Q

What hematologic side effect is associated with phenytoin?

A

Megaloblastic anemia due to folate deficiency

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47
Q

Why does phenytoin cause megaloblastic anemia?

A
  • Folate deficiency

- Specifically, phenytoin inhibits “intestinal conjugase,” an enzyme that converts folate into its absorbable form

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48
Q

What is the MOA of of phenytoin?

A

Na+ channel inactivation

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49
Q

What is the most important clinical distinction between Folate and B12 deficiency causing megaloblastic anemia?

A

Folate does NOT have associated neurologic symptoms

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50
Q

What is the important lab distinction between Folate and B12 deficiency?

A 
Folate= elevated HOMOCYSTEINE; normal MMA 
B12= elevated MMA and Homocysteine
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51
Q

What is the most common composition of a kidney stone?

A

Calcium oxalate

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52
Q

What is the sympathetic viserosomatic reflex for the kidneys?

A

T9-L1

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53
Q

How does the presentation of dermatomyositis differ from polymyositis?

A

BOTH cause symmetric proximal muscle weakness; however, dermatomyositis is also associated with:

1) Malar rash (similar to SLE)
2) Gottron papules (hands)
3) Heliotrope (erythematous periorbital rash)
4) Shawl and face rash
5) Mechanics hands

54
Q

What histologic finding is pathognomonic for alcoholic hepatitis?

A

Mallory bodies

55
Q

What are Mallory bodies?

A

Intracytoplasmic eosinophilic inclusions of damaged keratin filaments

56
Q

In terms of the clinical presentation, how do gastric ulcers and duodenal ulcers differ? What is the mnemonic to remember the difference?

A

Gastric ulcer= Greater with meals– causes weight loss
Duodenal ulcer= Decreased with meals–weight gain

*Referring to pain

57
Q

What is the most common skin cancer?

A

Basal cell carcinoma

58
Q

What is the metastatic potential of basal cell carcinoma?

A

BCC rarely metastesizes

59
Q

What histologically identified BCC?

A

“Palaside nuclei” i.e. rows of nuclei that are oriented parallal to each other

*Looks kind of like a picket fence

60
Q

What is the treatment for BCC?

A

Surgical resection

61
Q

What is the oxygen saturation of blood in the umbilical vein?

A

80%

62
Q

What is the approximate oxygen saturation of blood as is passes through the fetal foramen ovale?

A

65%

63
Q

What is the indication for CV4: Bulb decompression?

A

To increase the amplitude of the Cranial Rhythmic Impulse (CRI)

64
Q

How is Sarcoidosis characterized?

A

Immune-mediated NON-CASEATING granulomas

65
Q

What serum levels are classically elevated in Sarcoidosis?

A

1) ACE

2) CD4/CD8 ratio

66
Q

Compare and contrast the venous drainage of the right and left ovaries. What is the mnemonic to remember the difference?

A

“Left ovary takes the Longest way”

Left= left gonadal vein, left renal vein*, IVC 
Right= right gonadal vein, IVC
67
Q

What is the MOA of digoxin?

A

1) Direct inhibition of the Na+/K+ ATPase
2) This causes INDIRECT inhibition of the Na+/Ca++ exhanger
3) Ca++ (intracellular) is increased
Net= positive ionotropic effect

*Also, stimulates the vagus nerve leading to decreased heart rate

68
Q

What are the clinical indications for digoxin?

A

1) Heart failure
2) A-fib

*Note that digoxin has been shown to decrease length of stay s/p acute MI; however, it has not been shown to reduce mortality from post-MI HF

69
Q

What is the most common cause of acute neuropathy?

A

Guillain-Barre Syndrome

70
Q

What is the most common subtype of Guillain-Barre Syndrome?

A

Acute Inflammatory Demyelinating Polyradiculopathy

71
Q

How does Acute Inflammatory Demyelinating Polyradiculopathy typically present?

A
  • Ascending paralysis post infection, especially Mycoplasma pneumoniae or Campylobacter jejuni
  • May be associated with sensory abnormalities i.e. paresthesias
72
Q

What toxicities are associated with the sulfonamides?

A

1) Hypersensitivity reactions
2) Hemolysis if G6PD
3) Nephrotoxicity
4) Photosensitivity
5) Kernicterus in infants
6) Displace other drugs from albumin i.e. warfarin

73
Q

What is the cross-re-activity between sulfonamide antibiotics and warfarin?

A
  • Sulfonamides displace warfarin from albumin

- Warfarin effect is enhanced

74
Q

What is the most common primary heart tumor in children?

A

Rhabdomyoma

75
Q

What is the most common sarcoma in adults?

A

Liposarcoma

76
Q

What is the classic presentation of Lewy Body Dementia?

A
  • Dementia and VISUAL HALLUCINATIONS followed by
  • Parkinsonism

Think “haLewycinations”

77
Q

What histologic finding is associated with Lewy Body Dementia?

A

Alpha-synuclein

78
Q

What are the classic presentation of MEN1?

A

1) Pancreatic islet tumors (gastrinoma)
2) Parathyroid hyperplasia
3) Pituitary tumors

79
Q

What is a Gastrinoma?

A

Gastrin secreting tumor that causes high levels of acid and ulcer formation that is refractory to PPIs

80
Q

What is Kluver-Bucy Syndrome?

A

Bilateral amygdala lesion leading to disinhibited behavior including:

1) Hyperphagia
2) Hypersexuality
3) Hyperorality

81
Q

What is Kluver-Bucy Syndrome associated with?

A

HSV-1 infection

82
Q

What is the first line treatment for gestational DM refractory to dietary control?

A

Insulin

83
Q

What is nutation?

A

“Sacral flexion” with extension of the SBS

  • Dura falls caudad
  • Sacrum falls forward
84
Q

What is counternutation?

A

“Sacral extension” with flexion of the SBS

  • Dura moves cephalad
  • Sacrum extends backward
85
Q

What happens to the diameter of the head with counternutation?

A
  • Head will WIDEN slightly

- Anterior-posterior diameter will DECREASE

86
Q

What happens to the diameter of the head with nutation?

A
  • Head will NARROW slightly

- Anterior-posterior diameter will INCREASE

87
Q

What causes chylothroax?

A

Trauma or malignancy damaging the thoracic duct and allowing lymphatic fluid to leak into the thoracic cavity

88
Q

If malignancy is the etiology of chylothroax, what is the most common type of cancer that manifests as chylothorax?

A

Lymphoma

89
Q

What are the expected findings on thorocentesis for chylothroax?

A

Milky-appearing fluid with ELEVATED TRIGLYCERIDES

90
Q

Describe the pathogenesis of Goodpasture Syndrome.

A

Type II Hypersensitivity Syndrome with autoantibodies directed against the glomerular basement membrane and the alveolar basement membrane

91
Q

What is the classic presentation of Goodpasture Syndrome?

A

Hemoptysis leading to progressive crescentric glomerulonephritis and rapid renal failure i.e.

“Rapidly Progressive Glomerulonephritis (RPGN)”

92
Q

Aside from Goodpasture Syndrome, what are the other two etiologies of RPGN?

A

1) Granulomatosis with polyangiitis (Wegner’s Syndrome)

2) Microscopic polyangiitis

93
Q

How are the etiologies of RPGN differentiated?

A

c-ANCA and p-ANCA antibodies

94
Q

Work-up for RPGN shows positive c-ANCA antibodies. What is the diagnosis?

A

Wegner’s Syndrome or Granulomatosis with Polyangiitis

95
Q

Work-up for RPGN shows positive p-ANCA antibodies. What is the diagnosis?

A

Microscopic Polyangitis

96
Q

Work-up for RPGN is negative for c-ANCA and p-ANCA antibodies. What is the diagnosis?

A

Goodpasture’s Syndrome

97
Q

What is the basic design of a cross-sectional study? What is this study measuring?

A

Data is collected from a group to assess frequency of disease

*Prevalence

98
Q

What is the basic design of a case-control study? What is this study measuring?

A

Comparison of a group of people with disease to a group without

*Odds ratio

99
Q

What is the basic design of a cohort study?

A

Comparison of a group with a given exposure or risk factor to a group without

*Relative risk

100
Q

What is the enzyme defect in PCT?

A

Uroporphyrinogen decarboxylase

101
Q

What are the clinical manifestations of PCT?

A

Blistering cutaneous photosensitivity

*This is the most common porphyria

102
Q

What is the major risk factor associated with PCT?

A

Anything that increases iron e.g. iron supplementation

103
Q

What is the enzyme defect in acute intermittent porphyria?

A

Prophobilinogen deaminase

104
Q

What is the classic presentation of AIP?

A

5 P’s

1) Painful abdomen
2) Port wine colored urine
3) Polyneuropathy
4) Psychological disturbance
5) Precipitated by drugs

105
Q

What is the MOA of NSAIDs?

A
  • Reversible inhibition of COX-1 and COX-2

- Blocks prostaglandin synthesis/ “cyclic endoperoxides”

106
Q

What are the “cyclic endoperoxidese” that are decreased by NSAID inhibition of COX-1 and COX-2?

A

1) PROSTACYCLIN
2) Prostalgandins
3) Thromboxane

107
Q

What symptom is associated with acute Schistosomiasis?

A

“Swimmer’s itch dermatitis”

108
Q

What are clinical manifestations of infection with S. mansoni?

A

Bloody diarrhea and hepatosplenomegaly

109
Q

What are clinical manifestations of infection with S. haematobium?

A

Painless hematuria and SCC of the bladder (chronic)

110
Q

What is the treatment for Schistosomiasis?

A

Praziquantel

111
Q

What is the MOA of Praziquantel?

A

Increased Ca++ permability of fluke tegument

112
Q

What type of drug is Physostigmine?

A

Anticholinesterase

113
Q

What is the clinical indication for Physostigmine?

A

Anticholinergic toxicity

*Think physostigmine phyxes atropine overdose

114
Q

What is the mnemonic to remember the order of organs involved in fetal erythropoiesis?

A

Young Liver Synthesizes Blood

Yolk sac
Liver
Spleen
Bone marrow

115
Q

During what timeframe is the yolk sac responsible for fetal erythropoiesis?

A

3-8 weeks

116
Q

During what timeframe is the liver responsible for fetal erythropoiesis?

A

6 weeks to birth

117
Q

During what timeframe is the spleen responsible for fetal erythropoiesis?

A

10-28 weeks

118
Q

During what timeframe is the bone marrow responsible for fetal erythropoiesis?

A

18 weeks to adult

119
Q

Non-seminomatous testicular cancer can be associated with an elevation of what hormone?

A

B-hCG

120
Q

What are the sequelae of B-hCG elevation in nonseminomatous testicular cancer?

A
  • Ligand receptor cross reactivity with TSH

- Hyperthyroidism-like syndrome

121
Q

Define alogia.

A

Without speech

122
Q

Define avolition.

A

Apathy

123
Q

What spinal levels are associated with the adrenal glands?

A

T8-T10

124
Q

What does a positive McMurray’s Test indicate?

A

Tears in the posterior aspect of the meniscus

125
Q

What does the ductus arteriosus connect?

A

Fetal pulmonary artery to descending aorta

126
Q

What is the underlying genetic defect seen in Rett Syndrome? What sex is this disorder seen in?

A
  • Deletion of the MECP2 gene
  • X-linked inheritance

*Seen in GIRLS (boys die)

127
Q

What are the clinical manifestations of Rett Syndrome?

A

At age 1-4:

1) Regression
2) Loss of development
3) Loss of verbal abilities
4) Intellectual disability
5) Ataxia
6) Stereotyped hand-wringing

128
Q

What is a Dandy-Walker malformation?

A
  • Agenesis of the cerebellar vermis and cystic enlargement of the 4th ventricle
  • Cystic enlargement of the 4th ventricle fills the posterior fossa near the base of the skull
129
Q

What is the Dandy-Walker malformation associated with?

A

1) Hydrocephalus

2) Spina bifida

130
Q

What is the clinical manifestation associated with malformation of the vermis in a Dandy Walker malformation?

A

Truncal ataxia

131
Q

What are the suspected CSF findings in bacterial meningitis?

A
  • Increased opening pressure
  • Increased neutrophils
  • Increased protein (above 50 mg/dL)
  • Decreased glucose (below 40 mg/dL)
132
Q

What acid-base disturbances are expected in an ASA overdose?

A

1) Respiratory alkalosis early

2) Transition to mixed metabolic acidosis-respiratory alkalosis

ComBANK Review (2 decks)

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