WEEK #2 Flashcards

(132 cards)

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
What are the two classes of dopamine agonists used to treat PD?
1) Ergot 2) Non-ergot* *Preferred
26
What is the Ergot DA agonist used to treat PD?
Bromocriptine
27
What are the Non-ergot DA agonists used to treat PD?
1) PRAMIPEXOLE | 2) Ropinirole
28
What PD drugs prevent peripheral L-DOPA degradation by inhibiting COMT?
1) Entacapone | 2) Tolcapone
29
What is Polycythemia Vera?
Disorder of increased RBC mass (w/ increased WBC and platelets)
30
What genetic mutation is associated with PV?
JAK2
31
What are the classic symptoms of PV?
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
32
What is Essential Thrombocytosis?
Disorder of increased platelets
33
What are the clinical manifestations of Essential Thrombocytosis?
1) Bleeding | 2) Thrombosis
34
What is the characteristic finding on bone marrow biopsy of a patient with Essential Thrombocytosis?
Enlarged megakaryocytes
35
How will the labs of a patient with PV differ from Essential Thrombocytosis?
``` PV= increased RBC, WBC, and platelets ET= Increased platelets ```
36
Where is the insertion of the supraspinatus muscle?
Greater tubercle of the humerus
37
What is Whipple Disease?
Bacterial infection with Treponema whipplei causing a malabsorption syndrome
38
What finding is pathognomonic for Whipple Disease?
PAS positive foamy macrophages in the intestinal lamina propria
39
What are the clinical manifestations of Whipple Disease?
Malabsorption syndrome PLUS: 1) Cardiac symptoms 2) Arthralgias 3) Neurologic symptoms
40
What is the MOA of the thiazide diuretics?
Inhibition of Na+/Cl- reabsorption in the Distal Convoluted Tubule (DCT)
41
What is the effect of the thiazide diuretics on Ca++?
Decreased Ca++ excretion
42
What is the mnemonic to remember the various side effects associated with the thiazide diuretics?
HyperGLUC - Hyperglycemia - Hyperlipidemia - Hyperuricemia - Hypercalcemia Also, HYPOkalemic metabolic alkalosis and hyponatremia
43
What is the MOA of the loop diuretics?
Inhibition of the Na+/K+/2Cl- cotransport system in the thick ascending loop of Henle
44
What is the mnemonic to remember what happens to Ca++ with the loop diuretics?
"Loops lose Ca++"
45
What is the MOA of acetazolamide?
Carbonic anhydrase inhibitor
46
What hematologic side effect is associated with phenytoin?
Megaloblastic anemia due to folate deficiency
47
Why does phenytoin cause megaloblastic anemia?
- Folate deficiency | - Specifically, phenytoin inhibits "intestinal conjugase," an enzyme that converts folate into its absorbable form
48
What is the MOA of of phenytoin?
Na+ channel inactivation
49
What is the most important clinical distinction between Folate and B12 deficiency causing megaloblastic anemia?
Folate does NOT have associated neurologic symptoms
50
What is the important lab distinction between Folate and B12 deficiency?
``` Folate= elevated HOMOCYSTEINE; normal MMA B12= elevated MMA and Homocysteine ```
51
What is the most common composition of a kidney stone?
Calcium oxalate
52
What is the sympathetic viserosomatic reflex for the kidneys?
T9-L1
53
How does the presentation of dermatomyositis differ from polymyositis?
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
What histologic finding is pathognomonic for alcoholic hepatitis?
Mallory bodies
55
What are Mallory bodies?
Intracytoplasmic eosinophilic inclusions of damaged keratin filaments
56
In terms of the clinical presentation, how do gastric ulcers and duodenal ulcers differ? What is the mnemonic to remember the difference?
Gastric ulcer= Greater with meals-- causes weight loss Duodenal ulcer= Decreased with meals--weight gain *Referring to pain
57
What is the most common skin cancer?
Basal cell carcinoma
58
What is the metastatic potential of basal cell carcinoma?
BCC rarely metastesizes
59
What histologically identified BCC?
"Palaside nuclei" i.e. rows of nuclei that are oriented parallal to each other *Looks kind of like a picket fence
60
What is the treatment for BCC?
Surgical resection
61
What is the oxygen saturation of blood in the umbilical vein?
80%
62
What is the approximate oxygen saturation of blood as is passes through the fetal foramen ovale?
65%
63
What is the indication for CV4: Bulb decompression?
To increase the amplitude of the Cranial Rhythmic Impulse (CRI)
64
How is Sarcoidosis characterized?
Immune-mediated NON-CASEATING granulomas
65
What serum levels are classically elevated in Sarcoidosis?
1) ACE | 2) CD4/CD8 ratio
66
Compare and contrast the venous drainage of the right and left ovaries. What is the mnemonic to remember the difference?
"Left ovary takes the Longest way" ``` Left= left gonadal vein, left renal vein*, IVC Right= right gonadal vein, IVC ```
67
What is the MOA of digoxin?
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
What are the clinical indications for digoxin?
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
What is the most common cause of acute neuropathy?
Guillain-Barre Syndrome
70
What is the most common subtype of Guillain-Barre Syndrome?
Acute Inflammatory Demyelinating Polyradiculopathy
71
How does Acute Inflammatory Demyelinating Polyradiculopathy typically present?
- Ascending paralysis post infection, especially Mycoplasma pneumoniae or Campylobacter jejuni - May be associated with sensory abnormalities i.e. paresthesias
72
What toxicities are associated with the sulfonamides?
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
What is the cross-re-activity between sulfonamide antibiotics and warfarin?
- Sulfonamides displace warfarin from albumin | - Warfarin effect is enhanced
74
What is the most common primary heart tumor in children?
Rhabdomyoma
75
What is the most common sarcoma in adults?
Liposarcoma
76
What is the classic presentation of Lewy Body Dementia?
- Dementia and VISUAL HALLUCINATIONS followed by - Parkinsonism Think "haLewycinations"
77
What histologic finding is associated with Lewy Body Dementia?
Alpha-synuclein
78
What are the classic presentation of MEN1?
1) Pancreatic islet tumors (gastrinoma) 2) Parathyroid hyperplasia 3) Pituitary tumors
79
What is a Gastrinoma?
Gastrin secreting tumor that causes high levels of acid and ulcer formation that is refractory to PPIs
80
What is Kluver-Bucy Syndrome?
Bilateral amygdala lesion leading to disinhibited behavior including: 1) Hyperphagia 2) Hypersexuality 3) Hyperorality
81
What is Kluver-Bucy Syndrome associated with?
HSV-1 infection
82
What is the first line treatment for gestational DM refractory to dietary control?
Insulin
83
What is nutation?
"Sacral flexion" with extension of the SBS - Dura falls caudad - Sacrum falls forward
84
What is counternutation?
"Sacral extension" with flexion of the SBS - Dura moves cephalad - Sacrum extends backward
85
What happens to the diameter of the head with counternutation?
- Head will WIDEN slightly | - Anterior-posterior diameter will DECREASE
86
What happens to the diameter of the head with nutation?
- Head will NARROW slightly | - Anterior-posterior diameter will INCREASE
87
What causes chylothroax?
Trauma or malignancy damaging the thoracic duct and allowing lymphatic fluid to leak into the thoracic cavity
88
If malignancy is the etiology of chylothroax, what is the most common type of cancer that manifests as chylothorax?
Lymphoma
89
What are the expected findings on thorocentesis for chylothroax?
Milky-appearing fluid with ELEVATED TRIGLYCERIDES
90
Describe the pathogenesis of Goodpasture Syndrome.
Type II Hypersensitivity Syndrome with autoantibodies directed against the glomerular basement membrane and the alveolar basement membrane
91
What is the classic presentation of Goodpasture Syndrome?
Hemoptysis leading to progressive crescentric glomerulonephritis and rapid renal failure i.e. "Rapidly Progressive Glomerulonephritis (RPGN)"
92
Aside from Goodpasture Syndrome, what are the other two etiologies of RPGN?
1) Granulomatosis with polyangiitis (Wegner's Syndrome) | 2) Microscopic polyangiitis
93
How are the etiologies of RPGN differentiated?
c-ANCA and p-ANCA antibodies
94
Work-up for RPGN shows positive c-ANCA antibodies. What is the diagnosis?
Wegner's Syndrome or Granulomatosis with Polyangiitis
95
Work-up for RPGN shows positive p-ANCA antibodies. What is the diagnosis?
Microscopic Polyangitis
96
Work-up for RPGN is negative for c-ANCA and p-ANCA antibodies. What is the diagnosis?
Goodpasture's Syndrome
97
What is the basic design of a cross-sectional study? What is this study measuring?
Data is collected from a group to assess frequency of disease *Prevalence
98
What is the basic design of a case-control study? What is this study measuring?
Comparison of a group of people with disease to a group without *Odds ratio
99
What is the basic design of a cohort study?
Comparison of a group with a given exposure or risk factor to a group without *Relative risk
100
What is the enzyme defect in PCT?
Uroporphyrinogen decarboxylase
101
What are the clinical manifestations of PCT?
Blistering cutaneous photosensitivity *This is the most common porphyria
102
What is the major risk factor associated with PCT?
Anything that increases iron e.g. iron supplementation
103
What is the enzyme defect in acute intermittent porphyria?
Prophobilinogen deaminase
104
What is the classic presentation of AIP?
5 P's 1) Painful abdomen 2) Port wine colored urine 3) Polyneuropathy 4) Psychological disturbance 5) Precipitated by drugs
105
What is the MOA of NSAIDs?
- Reversible inhibition of COX-1 and COX-2 | - Blocks prostaglandin synthesis/ "cyclic endoperoxides"
106
What are the "cyclic endoperoxidese" that are decreased by NSAID inhibition of COX-1 and COX-2?
1) PROSTACYCLIN 2) Prostalgandins 3) Thromboxane
107
What symptom is associated with acute Schistosomiasis?
"Swimmer's itch dermatitis"
108
What are clinical manifestations of infection with S. mansoni?
Bloody diarrhea and hepatosplenomegaly
109
What are clinical manifestations of infection with S. haematobium?
Painless hematuria and SCC of the bladder (chronic)
110
What is the treatment for Schistosomiasis?
Praziquantel
111
What is the MOA of Praziquantel?
Increased Ca++ permability of fluke tegument
112
What type of drug is Physostigmine?
Anticholinesterase
113
What is the clinical indication for Physostigmine?
Anticholinergic toxicity *Think physostigmine phyxes atropine overdose
114
What is the mnemonic to remember the order of organs involved in fetal erythropoiesis?
Young Liver Synthesizes Blood Yolk sac Liver Spleen Bone marrow
115
During what timeframe is the yolk sac responsible for fetal erythropoiesis?
3-8 weeks
116
During what timeframe is the liver responsible for fetal erythropoiesis?
6 weeks to birth
117
During what timeframe is the spleen responsible for fetal erythropoiesis?
10-28 weeks
118
During what timeframe is the bone marrow responsible for fetal erythropoiesis?
18 weeks to adult
119
Non-seminomatous testicular cancer can be associated with an elevation of what hormone?
B-hCG
120
What are the sequelae of B-hCG elevation in nonseminomatous testicular cancer?
- Ligand receptor cross reactivity with TSH | - Hyperthyroidism-like syndrome
121
Define alogia.
Without speech
122
Define avolition.
Apathy
123
What spinal levels are associated with the adrenal glands?
T8-T10
124
What does a positive McMurray's Test indicate?
Tears in the posterior aspect of the meniscus
125
What does the ductus arteriosus connect?
Fetal pulmonary artery to descending aorta
126
What is the underlying genetic defect seen in Rett Syndrome? What sex is this disorder seen in?
- Deletion of the MECP2 gene - X-linked inheritance *Seen in GIRLS (boys die)
127
What are the clinical manifestations of Rett Syndrome?
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
What is a Dandy-Walker malformation?
- 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
What is the Dandy-Walker malformation associated with?
1) Hydrocephalus | 2) Spina bifida
130
What is the clinical manifestation associated with malformation of the vermis in a Dandy Walker malformation?
Truncal ataxia
131
What are the suspected CSF findings in bacterial meningitis?
- Increased opening pressure - Increased neutrophils - Increased protein (above 50 mg/dL) - Decreased glucose (below 40 mg/dL)
132
What acid-base disturbances are expected in an ASA overdose?
1) Respiratory alkalosis early | 2) Transition to mixed metabolic acidosis-respiratory alkalosis