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STEP 1 MIXED > Deck 2 > Flashcards

Deck 2 Flashcards

1
Q

What is MOA for interaction between GTN and phosphodiestrase inhibitors (sildenafil, vardenafil, tadalafil)?

A

GTN nitrates cause NO creation, smooth muscle relaxation and increase cGMP. cGMP is metabolized by phosphodiestrase

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2
Q

What is xeroderma pigmentosum? Pathogenesis?

A

Xeroderma pigmentosum
Excessive sensitivity to sunlight, freckles and ulcers
UV rays –>thymine dimers –> defective nucleotide exision repair (lack of UV specific endonuclease that excises damaged DNA)

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3
Q

Which polio vaccine causes most robust IgA response?

A

Live attenuated oral (Sabin)

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4
Q

Pathogenesis of hyper-IgM syndrome?

A

Defective CD40 (B cells) binding CD40L (T cells) so no class switching

Patients will have opportunistic infections

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5
Q

What causes acanthosis nigrans in DM?

A

Free fatty acids cause insulin resistance
Increase hepatic gluconeogenesis
Impair insulin-dependent glucose uptake

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6
Q

Which electrolytes are abundant inside vs outside cell?

A

K in cell

Na, Cl, Ca all extracellular

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7
Q

Which kidney cells increase potassium reabsorption in hypokalemia?

A

Alpha intercalcated cells

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8
Q

Which kidney cells increase K secretion in hyperkalemia?

A

Principal cells in collecting duct

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9
Q

What promotes increased K+ excretion?

A

High extracellular K+, increased aldosterone, alkalosis (promotes K entry into principal and alphaintercalcated cells), increased tubular flow (high sodium, volume expansion)

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10
Q

How does sarcoidosis cause hypercalcemia?

A

Activated macrophages express PTH independent conversaion of 1-alpha-hydroxylase, leading to increased conversion of vit D to 1,25 dihydrocalciferol

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11
Q

Which medication should you give acutely to people with contraindicated NSAIDs in gout?

What are SE of it?

A

Colchecine

N/v, diarrhea, abdo pain (disrupts microtubule formation in GI cells)
Impaired leukocyte migration and phagocytosis

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12
Q

What is Abetalipoproteinemia?

A

Autosomal recessive disease - can’t synthesize ApolipoproteinB. Foamy cytoplasm of enterocytes.

Malabsoprtion, greasy stools, abdominal distension
Low plasma triglycerides, cholesterol, VLDLs, and apoB. Poor lipid absorption

Caused by MTP gene mutation
RBCs show acanthocytes (thorny appearance) and neurological abnormalities

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13
Q

Where is SA node anatomically?

A

RA near superior vena cava

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14
Q

Where is AV node anatomically?

A

RA near tricuspid valve

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15
Q

Where should thoracocentesis be performed in front, middle and back?

A

Midclavicular 6-8 ribs
Midaxillary 8-10
Posterior 10-12

Anything below these risks penetrating abdominal structures

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16
Q

Where do nerve, artery, and vein lie between ribs?

A

On the lower border of the rib

Always perform thoracocentesis on the upper border

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17
Q

What drug class is scopolamine?

A

Antimucarinics (anticholingergis)

Motion sickness

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18
Q

What drug class is Diphenhydramine, meclizine, and promethazine?

A

Antihistamines

Motion sickness and hyperemesis gravidarum

19
Q

What drug class is prochloperazine and metclopramide?

A

Dopamine receptor antagonists

Chemotherapy induced emesis

20
Q

What drug class is ondasteron and granisetron?

A

Serotonin 5-HT3 receptor antagonists

Chemotherapy induced emesis

21
Q

What class of drug is aprepitant and posaprepitant?

A

Neurokinin 1 (NK1) receptor antagonist

Chemotherapy induced emesis

22
Q

What areas of the brain are involved in vomiting?

A 
Area postrema (floor of 4th entircle)
NTS (Medulla)
23
Q

What receptors are involved in vomiting?

A

H1, 5-HT3, D2, M1, NK1,

24
Q

What agent should be used in pregnant women with DVT?

A

LMWH (enoxaparin) heparin doesn’t cross placenta

25
Q

What is found on histology for histoplasma infection?

A

Granulomas, macrophages with intracellular oval yeast

26
Q

What are short acting post parandial insulins?

A

Aspart, lispro, glulisine

27
Q

What are long acting insulins?

A

Detemir, glargine

28
Q

Baby with bloody stools, abdominal distention, and air in bowel wall. What is it?

A

nec enterocolitis

29
Q

What pharyngeal arches are innerved by what nerves?

A

Arch 1 - CN V
Arch 2- CN VII
Arch 3 CN IX
Arch 4 & 6 CN X

30
Q

What does the 1st pharyngeal arch become?

A

Muscles of mastication, Zygoma, Incus, Malleus, maxillary bone, mandible

31
Q

What does 2nd pharyngeal arch become?

A

Muscles of facial expression, Stapes, styloid, lesser horn of hyoid

32
Q

What is Treacher-Collins syndrome?

A

Abnormal development of 1st and 2nd pharyngeal arches. Craniofacial abnormalities, airway compromise, absent middle ear bones

33
Q

What are symptoms of atypical depression?

A

Mood reactivity, rejection sensitivty, increased sleep and appetite, leaden paralysis

34
Q

What meds are used to treat atypical depression?

A

MAOIs (phenelzine)

35
Q

When to use MAOIs in depression?

A

Treatment resistant depression or atypical features of MDD

36
Q

What causes hematuria and elevated urine pH?

A

Struvite stones

37
Q

What receptors dialate pupil?

A

Alpha 1 agonists

38
Q

Which receptors relax uterus?

A

B2 agonists such as terbutaline and ritodrine (used as tocolysis)

39
Q

What drugs cause tosades de pointes? MOA?

A

Prolong QT interval

Class IA and III antiarrhythmics (sotalol, quinidine)
antipsychotics (haloperidol)
Antibiotics (macrolides, quinolones)

40
Q

What are clinical manifestations of primary ciliary diskynesia?

A

Infertility- sperm motility impaired
Chronic sinusitis, bronciectesis
situs inversus

41
Q

What causes hemibalism?

A

Damage to subthalamic nucleus (part of basal ganglia), usually from lacunar stroke due to HTN or diabetes

42
Q

What part of brain mediates satiety?

A

Ventromedial hypothalamic nuclei. Damage leads to hyperphagia and obeisity

43
Q

What part of hypothalamus mediates hunger?

A

Lateral hypothalamic nuclei

STEP 1 MIXED (13 decks)

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