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Review / Wrong Answers > 6/16 UWorld > Flashcards

6/16 UWorld Flashcards

1
Q

What is the difference between simple focal and complex focal seizures

A
  • Simple
    • No LOC or postictal state
    • Motor, sensory, autonomic, or psychic symptoms
  • Complex
    • LOC and postictal state
    • May have automatisms (e.g. lip smacking)
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2
Q

Describe presentation of tonic-clonic vs. myoclonic seizure

A
  • Tonic-clonic
    • LOC and postictal state
    • Diffuse muscle contraction of limbs (tonic) followed by rhythmic jerkin (clonic)
  • Myoclonic
    • No LOC or postictal state
    • Brief jerking movements
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3
Q

What are the broad spectrum anti-epileptics that can be used to treat focal, tonic-clonic, and absence seizures

A

Valproic acid

Lamotrigine

Recall festival and Llamas outside of Ethosuximide classroom

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4
Q

First line therapy for absence seizures

A

Ethosuximide

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5
Q

First line treatment for focal seizures

A

Carbamazepine

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6
Q

First line treatment for tonic-clonic seizures

A

Phenytoin, Valproic acid

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7
Q

First line treatment for status epilepticus

A

Phenytoin - 1st line prophylaxis

Benzos - 1st line for acute

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8
Q

MOA and uses of Gabapentin

A
  • SKetchy = Grab a pint ice cream truck
  • Mechanism of action:
    • Narrow spectrum anti-epileptic
    • Bind and block voltage-gated calcium channels, stopping inward calcium current, stopping NT release
    • Does NOT bind to GABA receptors
  • Uses:
    • Anti-seizure
    • Neuropathic pain (e.g. diabetic neuropathy)
    • Fibromyalgia
    • Post-herpetic neuralgia (VZV)
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9
Q

MOA and uses of Vigabatrin

A
  • Sketchy = V cab
  • Narrow spectrum antiepileptics
  • Mechanism of action:
    • Irreversible inhibitor of GABA-transaminase, enzyme responsible for degradation of GABA
      • = raised CAB
      • = V cab “transmission”
    • This produces and increase of GABA in the CNS, producing tonic inhibition
  • Uses:
    • Adjunctive treatment for partial seizures
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10
Q

MOA and uses of Tiagabine

A
  • Sketchy = tied up cab driver
  • Narrow spectrum antiepileptics
  • Mechanism of action:
    • Inhibits GABA reuptake, increasing GABA concentration in CNS
  • Uses:
    • Adjunctive treatment for partial seizures
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11
Q

Cause and presentation of Hyper IgE syndrome

A

o Deficiency in IFN-y lead to impaired neutrophil recruitment

o Presentation à FATED

§ F – coarse Facies

§ A – Abscesses

§ T – retained primary Teeth

§ E – increased IgE (all other immunoglobulins are normal)

§ D – dermatologic problems (eczema)

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12
Q

Release and function of TNF-a

A

§ Secreted by activated macrophages

§ Mediates septic shock

§ Causes neutrophil and lymphocyte recruitment

§ Responsible for fever, anorexia, corticotrophin releasing hormone, septic shock, and cachexia

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13
Q

MOA and uses of Infliximab

A
  • THINK: TNF = The NetFLIX Friday
  • TNF-a inhibitor
    • Recall: TNF-a is an acute phase reactant produced by activated macrophages to mediate inflammation by accelerating neutrophil migration, and facilitate lymphocyte proliferation; TNF-a is responsible for fever, anorexia, corticotropin releasing hormone, septic shot, and cachexia
  • Mechanism of action:
    • Is a monoclonal antibody to TNF-a
  • Uses:
    • Used for autoimmune conditions due to anti-inflammatory effect
    • Rheumatoid arthritis, psoriasis, ankylosing spondylitis
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14
Q

What are the 2 drugs that inhibit IL-2 transcription

A

Cyclosporine and Tacrolimus

  • THINK: you use a toilet paper roll (Tacrolimus) to make yourself look like a cyclops (Cyclosporine) instead of having 2 eyes (IL-2)
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15
Q

What 2 drugs prevent IL-2 response

A

Sirolumus and Dacluzimab

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16
Q

What is the use of drugs that inhibit IL-2

A

Transplant rejection prophylaxis, psoriasis, rheumatoid arthritis

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17
Q

Describe the defect and presentation fo Wiskott Aldrich syndrome

A

o X-linked recessive immunodeficiency due to mutation in WASp gene

o Leukocytes and platelets unable to reorganize actin skeleton = defective antigen presentation

o WATER - Wiskott Aldrich, Thrombocytopenia, Eczema (especially truncal), Recurrent infections

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18
Q

Antibody associated with mixed connective tissue disease

A

Anti-U1 RNP (ribonucleoprotein)

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19
Q

What are the different defects that cause homonymous hemianopia with macular involvment vs homonymous hemianopia with macular sparing

A

E: homonymous hemianopia with macular involvement is consistent with involvement of the temporal lobe (e.g. occlusion of the middle cerebral artery)

H: homonymous hemianopia with macular sparing is consistent with occlusion of the posterior cerebral

20
Q

When after fertilization will b-hCG become positive in materal serum vs. urin

A

8 days = serum

14 days = urine

21
Q

What murmur is associated with an opening snap vs. an ejection click

A

Opening snap = mitral stenosis

Ejection click = aortic stenosis

22
Q

What is the most common location of patients infected with Babesia

A

NE United States (NE on maltese cross on floor)

23
Q

Presentation of carcinoid syndrome

A
  • Symptoms = BFDR
    • Bronchospasm
    • Flushing
    • Diarrhea
    • Right-sided heart disease/murmur
24
Q

Where is the inflammation and with what T-cell (CD4+ or CD8+) is inflammation caused by in Dermatomyositis vs. Polymyositis

A
  • Dermatomyositis
    • Perimysial (THINK: periphery b/c of muscle + skin involvement) inflammation with CD4+ T cells
  • Polymyositis
    • Endomysial inflammation with CD8+ T cells
    • Think of the 8 as multiple bulging muscles
25
Q

What human leukocyte antigen is associated with the seronegative spondyloarthropathie

A

HLA-B27

26
Q

What human leukocyte antigen is associated with Rheumatoid arthritis

A

HLA-DR4

Think of a doctor kneeling on the floor

27
Q

Where do each of the 6 EKG leads point? (aVR, aVF, aVL, I, II, III)

A
28
Q

What leads will you see affected in an infarct to each of the following areas:

  • Lateral heart (LCX)
  • Anterior/septal heart (LAD)
  • Inferior heart (RCA)
A
  • Lateral (LCX) = I, aVL
  • Anteroseptal infarct (LAD) = V1-V4
  • Inferior (RCA) = II, III, aVF
29
Q

Hormones that use the cAMP pathway (Gs and Gi)

A
  • Most hormones of anterior pituitary
  • FSH, LH, ACTH, TSH, hCG, MSH, GHRH, CRH, PTH, calcitonin, glucagon, V2 vasopressin receptor
  • THINK: FLAT ChAMP
    • FSH, LH, ACTH, TSH, CRH and calcitonin, hCG, ADH (V2), MSH, PTH
30
Q

Hormones that use the IP3 pathway

A
  • Hormones of posterior pituitary minus V2
  • GnRH, TRH, oxytocin, V1 vasopressin receptor, H1 histamine receptor, angiotensin II, gastrin
  • THINK: GOAT HAG
    • GnRH, Oxytocin, ADH (V1), TRH, Histamine (H1), Angiotensin II, Gastrin
31
Q

Hormones that have steroid receptos

A
  • Estrogens, progesterone, testosterone, glucocorticoids, aldosterone, thyroid hormone (T3/T4), vitamin D
  • THINK: VETTT CAP
    • Vitamin D, Estrogen, Testosterone, T3, T4, Cortisol, Aldosterone, Progesterone
32
Q

Hormones with tyrosine kinase receptors

A
  • Insulin, insulin-like growth factor (IGF-1), platelet derived growth factor (PDGF), fibroblast growth factor (FGF)
    • THINK: insulin + all the –GF’s
33
Q

Hormones with non-receptor tyrosine kinase (JAK/STAT)

A
  • Prolactin, cytokines (IL-2, IL-6, IFN), GH, G-CSF, Erythropoietin, Thrombopoeitin
  • THINK: PIGGLET
    • Prolactin, Immunomodulators (cytokines, IL-2, IFN), Growth hormone, Granulocyte colony stimulating factor, (No L), EPO, Thrombopoietin
34
Q

MOA of Docusate

A

Stool softener

Facilitates the penetration of stool by water and lipids

35
Q

MOA of Bismuth

A

MOA:
Binds to ulcer base, providing physical protection and allowing HCO3- secretion to reestablish pH gradient in the mucus layer

USES:
Increased ulcer healing
Traveler’s diarrhea

36
Q

MOA of Exanatide and Liraglutide

A

“-tide” = GLP-1 agonists

  • These drugs activate GLP-1 receptor (glucagon-like peptide receptor) – opposite of glucagon
    • Increases insulin release and satiety
    • Decreases glucagon release and gastric emptying
37
Q

MOA of Sitagliptin and Linagliptin

A

“-gliptin” = DDP-4 inhibitors

  • DPP-4 (dipeptidyl peptidase) is the enzyme that breaks down endogenous GLP-1
  • If you inhibit DPP-4, you will have more endogenous GLP
    • Increased insulin and decreased glucagon
    • Increased satiety and delayed gastric emptying
38
Q

MOA of Pramlintide

A
  • Amylin analog
  • Amylin is a peptide normally present in insulin secretory granules and secreted along with insulin
    • At pharmacologic doses, it reduces glucagon secretion, gastric emptying, and appetite
  • Used to control postprandial glucose spike in both Type I and Type II DM
39
Q

MOA of alpha-glucosidase inhibitors (Acarbose and Miglitol)

A

Sketchy: A-carb wigglers

MOA:
Inhibition of a-glucosidase on the intestinal brush border decreases the conversion of disaccharides to absorbable monosaccharides –> delayed carbohydrate absorption

USES:
Type 2 DM

ADVERSE EFFECTS:
Diarrhea, flatulence (due to fermentation of undigested carbs)

40
Q

MOA of SGLT2 inhibitors (“-flozin”)

A

Sketchy: Flossing teacher and Salty Glucose Co. bag

MOA:
Inhibition of the sodium-glucose cotransporter in the proximal tubule

USES:
Type 2 DM

ADVERSE EFFECTS:
UTI
Vaginal candidiasis
Dehydration

41
Q

What are the rapid-acting, intermediate-acting, and long-acting insulins

A
  • Rapid acting = Girls and Lads
    • Glulisine, Aspart, Lispro
  • Intermediate acting = Rest Now
    • Regular insulin, NPH
  • Long acting = Don’t Go
    • Detemir, Glargine
42
Q

Describe the different effects on Phase 0 slope and effective refractory period of Class IA, IB, and IC antiarrhythmics

A
  • Class IA:
    • Intermediate Na+ channel binding – moderately decreased phase 0 slope
    • Also block K+ channels – prolonged refractory period
  • Class IB:
    • Weakest Na+ channel binding – minimally decreased phase 0 slope
    • Cause shortened refractory period
  • Class IC:
    • Strongest Na+ channel blocking – significantly decreased phase 0 slope
    • No effect on refractory period
43
Q

Describe what part of the action potential each class of Anti-arrhythmics works on (which electrolyte channel and which phase)

A

THINK: No Bad Boy Keeps Clean

  • Class I
    • Na+ channel blockers
    • Phase 0 of myocytes
  • Class II
    • Beta blockers
    • Phase 4 of pacemakers
  • Class III
    • K+ channel blockers
    • Phase 2 and 3 of myocytes
  • Class IV
    • Ca2+ channel blockers
    • Phase 0 of pacemakers
44
Q

What drugs are Class III anti-arrhythmics

A
  • Amiodarone
    • = Amigos
  • “-tilide” suffix (e.g. Dofetilide and Ibutilide)
    • = “til I die” note
  • Sotalol
    • = soda
      • Is also a beta blocker (-lol suffix)
      • Muted bugle
45
Q

What are the Class I antiarrhythmics (IA, IB, IC)

A

IA - Quinidine, Procainamide, Disopyramide

IB - Lidocaine, Mexiletine, Phenytoin

IC - Flecainide, Propafenone

46
Q

Are the Class IV anti-arrhythmics dihydropyridines or non-dihydropyridines

A

Non-dihydropyridines

Review / Wrong Answers (140 decks)

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