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First Pass Miss Step 1 > Don't Know At All > Flashcards

Don't Know At All Flashcards

1
Q

What is the mechanism of action of glycopyrrolate?

A

Antimuscarinic - used to reduce airway secretions pre-op, before intubation

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2
Q

What is the mechanism of action of midodrine and its used?

A

Alpha1 agonist, used in the treatment of autonomic insufficiency leading to orthostatic hypotension

mid”O”drine = “O”rthostatic hypotension

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3
Q

What are two key side effects of nitrofurantoin?

A
  1. Pulmonary fibrosis

2. Hemolysis in G6PD deficiency

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4
Q

What is a Warthin-Finkeldey cell?

A

A fused lymphocyte giant cell, usually caused by the fusion protein of Measles (Rubeola)

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5
Q

How do Bunyaviruses get their envelope? What’s the structure of the genome?

A

Gold bathrobe -> Golgi apparatus

RNA negative virus with three CIRCULAR segments (think of the three chopped down tree stumps with rings)

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6
Q

What type of virus is Zikavirus? What is its symptom other than congenital microcephaly?

A

Flavivirus transmitted by Aedes mosquito (like Dengue fever)

Symptom - conjunctivitis

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7
Q

Give two ways S. bovis is told apart from enterococcus?

A
  1. S. bovis cannot grow in 6.5% NaCl

2. S. bovis is PYR negative while enterococcus is PYR positive.

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8
Q

What are the important class side effects of NNRTIs? Efavirenz?

A
  1. Hepatotoxicity - seen in all - think of the horse with the liver spot
  2. SJS / rash - think of the SJS mask on the left side of the picture

Efavirenz - CNS toxicity / psychiatric disturbance

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9
Q

What is the main toxicity of cidofovir and how do you reduce this?

A

Nephrotoxicity
-> reduce by giving with probenecid -> think of the probation officer keeping cid away from the shelf of kidneys

Also give IV saline to keep hydration up (like amphotericin)

Giving probenecid reduces the renal excretion of cidofovir, preventing high tubular concentration and subsequent kidney damage.

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10
Q

What are the mechanisms of permethrin, malathion, and lindane?

A

PML will NAG you

Permethrin - Na+ blockade
Malathion - Acetylcholinesterase inhibitor
Lindane - GABA channel blocker -> neurotoxicity

Used against mites and lice

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11
Q

What syndrome does Foxp3 mutation cause? Symptoms?

A 
IPEX
Immune dysregulation,
Polyendocrinopathy - thyroiditis and pancreatitis -> destruction of pancreatic islets
Enteropathy - diarrhea
X-linked - (diabetes in males infants)

Also has dermatologic manifestations i.e. dermatitis / nail dystrophy

Think XP3 = IP3X

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12
Q

What is endocardial fibroelastosis and who is it seen in?

A

A condition of thickening of the endocardium, seen in young children
-> rare cause of restrictive cardiomyopathy

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13
Q

What do you think about an adult with asthma, nasal polyps, and bronchospasm?

A

Likely aspirin-induced asthma - seen in 10% of adults

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14
Q

What happens when TB involves the kidneys?

A

Causes a sterile pyuria

Dr. Sattar says it’s common

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15
Q

How does the pulmonary artery relate to the bronchus at each lung hilum?

A

Think RALS

Right - Anterior
Left - Superior

Right pulmonary artery is anterior to the right mainstem bronchus

Left pulmonary artery is superior to the left mainstem bronchus

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16
Q

What gives rise to the middle ear bones vs sensory organs of the ear (i.e. cochlea)

A

Middle ear ossicles / muscles -neural crest

Inner ear - Otic placodes (from ectodermal placodes)

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17
Q

What are the congenital and acquired causes of sideroblastic anemia? Pattern of inheritance?

A

Congenital - X-linked! ALA synthase mutation
Acquired:
1. Alcohol - mitochondrial poison
2. Lead - inhibits ALA dehydratase and ferrochelatase
3. B6 deficiency - usually due to isoniazid therapy - ALAS deficiency
4. Myelodysplastic syndromes - screws up synthesis

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18
Q

What is an example of a nonmegaloblastic macrocytic anemia? A couple more example causes?

A

Diamond-Blackfan anemia -> rapid onset anemia in 1st year due to intrinsic erythroid defect, increased %HbF but decreased total Hb. Craniofacial abnormalities and triphalangeal thumbs (very similar to Fanconi anemia).

A couple more:

  1. Alcohol - can cause macrocytic (bone marrow suppression) or megaloblastic (folate deficiency)
  2. Liver disease - mechanism uncertain
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19
Q

What test can be used to screen if patients have HbS of any amount?

A

Metabisulfite screen - positive in both disease and treat by inducing sickling

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20
Q

What marker will be decreased on neutrophils during a left shift?

A

Immature neutrophils have impaired expression of CD16

  • > CD16 = Fc receptor.
  • > Don’t function as well for phagocytosis and antibody-dependent cell mediated cytotoxicity
  • > also present on NK cells
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21
Q

What can Adult T cell leukemia/lymphoma be easily confused with and how do you differentiate?

A

Easily confused with multiple myeloma, since it also causes lytic bone lesions and hypercalcemia

  • > differentiate based on presence of rash
  • > T cell lymphomas love to go to the skin and cause rash
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22
Q

What is the Jak1/Jak2 inhibitor which can be used in myeloproliferative disorders with Jak2 mutations?

A

Ruxolitinib

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23
Q

How do you distinguish primary myelofibrosis from hairy cell leukemia?

A
  1. Primary myelofibrosis is more likely to have normal WBC and platelet counts. (HCL causes pancytopenia)
  2. Dacrocytes / tear drop cells will also be seen due to RBCs being squeezed out of fibrosed bone marrow in PMF, but are NOT seen in HCL.
  3. Hairy cell leukemia will show hairy B cells which are TRAP+.
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24
Q

What is the main indication for factor Xa inhibitors and what are they?

A

ApiXaban, rivaroXaban

  • > used as direct oral anticoagulants (DOACs) for longterm DVT and PE prophylaxis, as well as stroke prevention in AFib
  • > the only direct thrombin inhibitor which is a DOAC is the one with a reversal agent: Dabigatran.

Direct THROMBIN inhibitors are used for HIT

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25
Q

What are the common toxicities of sunitinib?

A

Hyperkeratosis / rash - out in the hot sun
Hypertension (like bevacizumab) - due to inhibition of VEGF. This is more high yield (to know for the purposes of board examinations!) than sketchy’s hemorrhage side effect.

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26
Q

What does LM and DIF show in membranous nephropathy?

A

LM - diffuse capillary wall THICKENING (membranous) with NORMOcellular glomeruli

DIF - Lumpy bump, granular appearance with immune complex deposition (IgG and complement, but not recruiting more cells)

EM - “spike and dome” appearance as spikes of GBM encircle the immune complexes (membrane is proliferating, forming a DOME), with spikes separating the immune complex domes.
-> subEPIthelial immune complex deposition (vs MPGN1/2)

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27
Q

Which types of stones are particularly prone to precipitate in acidic urine?

A

Uric acid stones, cystine stones
-> both types are radiotranslucent and can be treated with acetazolamide for alkalinization

Calcium OXALATE stones are also associated with acidic urine, but not precipitated by it
-> since acidic urine proximally is associated with increased citrate resorption -> increased calcium oxalate stone risk.

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28
Q

What cells are an oncocytoma comprised of? What must they be differentiated from? Is it benign or malignant?

A

Comprised of oncocytes - renal collecting duct intercalated epithelial cells (distal collecting duct, for H+/K+ exchange) which stain very eosinophilically due to abundant mitochondria and lack of perinuclear clearing (vs chromophobe RCC part of Birt-Hogg-Dube)

It is a benign tumor

29
Q

What is the cause of stress incontinence and what conditions does it exist in?

A

Outlet incompetence (i.e. intrinsic sphincteric deficiency due to trauma or pudendal nerve injury in childbirth, or urethral hypermobility)

  • > often happens in pregnancy, obesity, or post-vaginal deliver
  • > coughing or Valsalva manuever (increased intraabdominal pressure / stress) -> leakage of urine.

vs urge (MS) / overflow (diabetes)

30
Q

What might exogenous vasopressin (not desmopressin) be specifically useful for?

A

Treatment of esophageal varices -> V1 receptor can constrict these veins. -> think of the blue golf club guy with ADH backpack next to the V1 receptors

-> along with octreotide, nadolol, and propranolol

31
Q

What is the triad of Behcet syndrome?

A
  1. Recurrent aphthous ulcers
  2. Genital ulcers
  3. Uveitis causing visual disturbances
    - > etiology is unknown
32
Q

What chromosome is FAP on?

A

5 = i fap with my 5 fingers

33
Q

Where does pain radiate in acute cholecystitis?

A

Right scapula - and that is high yield

34
Q

How does alcoholic hepatitis appear pathologically? What causes this? What is the major distinguishing feature from viral hepatitis?

A

Swollen and necrotic hepatocytes with a NEUTROPHILIC inflammatory infiltrate (vs viral = lymphocytic).

Mallory-Denk bodies -> alcoholic hyaline - eosinophilic cytoplasmic inclusions which are inclusions of damage keratin filaments (intermediate filaments!)

Consider that Mallory-Weiss and Mallory-Denk are both alcohol related - Mallory Mager

35
Q

How does point of service (POS) differ from health maintenance organization (HMO)?

A

Both require PCP referrals to see a specialist, but point of service is allowed to see doctors outside of the preferred network, where HMO patients must stay in network

36
Q

What measure is (1 - false positive rate)? How do you calculate?

A

Specificity!
True negative rate = TN / (TN + FP)
(No disease and test is negative) / (No disease and test is negative + No disease and test is positive)

= d / b+d

37
Q

How does PPO differ from EPO?

A

EPO = exclusive provider organization, patients must stay within a network but do not need a PCP referral

PPO = patients do not need PCP referral and can see out of network

EPO is to PPO as HMO is to POS.

38
Q

When are likelihood ratios useful and what determines if something is a very useful diagnostic test with these ratios?

A

Useful when the prevalence is unfavorable for dealing with PPV / NPV -> tells you the utility of just the test alone.

+LR > 10 is a useful test to rule in
-LR < 0.1 is a useful test to rule out

39
Q

How do you calculate positive likelihood ratio?

A

LR+ = sensitivity / (1-specificity) = true positive rate / false positive rate.

Notice that this is very similar to the calculation of PPV, just doesn’t depend on prevalence in the population. It is the RATE of true positives / RATE of false positives.

40
Q

What is the formula for average duration of disease in terms of prevalence and incidence?

A

(Prevalence) / (1-Prevalence) = Incidence * Average duration of disease

You can think of this as:
(number of people with it) / (number of people susceptible) = rate of new cases among susceptible * disease duration

This is the steady state equation for a population

proportion = proportion / time * time

http://sphweb.bumc.bu.edu/otlt/MPH-Modules/EP/EP713_DiseaseFrequency/EP713_DiseaseFrequency7.html

41
Q

What would be the formula for a 95% and 99% confidence interval in a study with mean 10 and standard deviation of 3, with sample size 100

A

z score for 95% = 1.96
z score for 99% = 2.58

sample mean +/- zscore * standard error

standard error = 3/sqrt(100) = 0.3

10 +/- 1.96*0.3 = 10+/-0.588. We are 95% confident that the true population mean lies within this interval.

42
Q

How do you differentiate between syphilis condylomas and HPV condylomas

A

Syphilis tends to be fLat

HPV is cauliflower like

43
Q

What condition is associated with dilated cardiomyopathy with APICAL ATROPHY?

A

Chagas disease

44
Q

How are Pick-bodies known for being stained and looking?

A

Silver-staining, spherical aggregation of Tau proteins

45
Q

What is a waxy cast caused by?

A

Often a broad cast, it is due to chronic renal failure and the degeneration of granular casts in hypertrophied tubules

-> vs Hyaline casts which are seen in concentrated urine samples

46
Q

What is primary vs secondary vs tertiary vs quaternary prevention?

A

Primary - Prevent (i.e. vaccination)
Secondary - Screen for asympatomatic (i.e. Pap smear)
Tertiary - Treat to reduce complications
Quaternary - prevention of unnecessary treatment / interventions by properly sharing test results

47
Q

What are the four parts of medicare?

A

A - HospitAl insurance / home hospice care
B - Basic medical bills (i.e. doctors fees and preventative care)
C - delivery by approved private Companies (Combo of A + B)
D - Drugs

48
Q

When is Medicare available to patients?

A

Age 65

those with certain disabilities <65

49
Q

What is a Failure mode and effects analysis?

A

Usage of inductive reasoning and forward-looking approach to determine what’s likely to fail and what’s most important to fix first.

Root cause analysis is different, it’s retrospective (after an event occurred).

50
Q

What liver enzymes suggest alcoholic liver damage vs viral hepatitis?

A

Elevated AST > ALT, ratio of AST:ALT is increased.

Also, elevated GGT levels

  • > this makes sense because y-glutamyltransferase is a marker for ductal damage, and impairs ductal secretions
  • > this is why alcohol can cause pancreatitis
51
Q

What effect do benzos have on REM sleep?

A

Like alcohol, they decrease REM sleep

and deep sleep

52
Q

How does oil:gas partition coefficient relate to induction speed, recovery time, potency, and MAC?

A

Increased solubility in lipids = increased potency = lower minimum alveolar concentration required to induce (potency is inversely proportional to MAC)

Lipid solubility has no relation to induction speed / recovery time

53
Q

Which TCAs are known for having more or less anticholinergic effects?

A

Tertiary amines - i.e. AmiTRIptyline -> easier binds and inhibits the tertiary amine acetylcholine

Secondary amines - think NORth side prep secondary school -> Nortriptyline / desipramine have less cholinergic effects due to binding less tightly.

54
Q

What is the only opiate which causes mydriasis and when must you also be careful when using it?

A

Meperidine (demerol)

  • > due to inhibition of NET/DAT
  • > also has weak serotonergic properties -> may precipitate serotonin syndrome when used with a MAO
55
Q

What is the mechanism of action of Vilazodone? What is its increased side effect?

A

SPARI - Serotonin partial agonist / reuptake inhibitor

SSRI + 5HT1A agonist -> possible increased efficacy for anxiety / depression

May make GI side effects worse

56
Q

What is the mechanism of action of aripiprazole?

A 
D2 partial agonist (blocks dopamine if there's alot)
5HT2A antagonism (accounts for effects)
5HT1A partial agonist -> like buspirone

More activating than other antipsychotics

57
Q

What is used for acute treatment and prophylaxis in cluster headache?

A

Acute - 100% oxygen therapy and sumatriptan (think of the cluser of lanterns above)
-> the fact that it’s in the sketch tells you sumatriptan can be used for this reason

Prophylaxis - Verapamil preferred (makes no sense, cerebral vasodilation but a non-DHP)

58
Q

When can amitriptyline be used for headache prevention?

A

Migraines AND tension headaches

Use verapamil for cluster headaches.

59
Q

What is a blackhead vs a whitehead?

A

These are NON-inflammatory processes
1. Open comedone - blackhead - where pore is plugged with keratin debris and oxidation turns it black

  1. Closed comedone - whitehead - the black part becomes hidden and skin grows overtop. Note, NOT a pustule.
60
Q

What is an ephelis and what causes it?

A

Freckle - a tan-brown macule which darkens with sunlight

Due to increased number of melanoSOMES, but the melanoCYTES are NOT increased.
-> vs. a nevus where melanocytes are increased

61
Q

What is bullous impetigo, and what is the cause of the systemic form of this disease?

A

Bullous impetigo is the localized form of SSSS, which in this case you would be able to culture S. aureus locally

Systemic form is SSSS, and is caused by toxins circulating throughout body distant from site of infection.
-> Staphylococcal exfoliative toxins cause INTRAepidermal splitting by cleaveage of desmoglein 1 in desmosomes

will heal without scarring, same pathology as pemphigus vulgaris! Nikolsky sign positive!

62
Q

What are the histologic features of lichen sclerosis?

A

Thinning of the epidermis - Atrophy of epidermis with absence of epidermal ridges

Fibrosis of the dermis - Replacement of underlying dermis with dense fibrotic collagenous connective tissue

-> Lichen Simplex Chronicus is the one due to chronic itching

63
Q

What is the hallmark of chronic endometritis and what are some common causes?

A

PLASMA CELLS in the stroma as part of chronic inflammation, as lymphocytes and macrophages are often present in endometrial stroma

Causes:
Pelvic inflammatory disease
Retained gestational products
IUDs -> A. israelii
TB -> will show granulomatous inflammation
64
Q

What is the other type of endometrial cancer and who tends to get it? Prognosis?

A

Sporadic endometrial cancer -> Type 2, occurs in older (wayyyy postmenopausal women, i.e. 70s/80s), no associated with estrogen
-> Occurs in the setting of atrophic endometrium with no precursor lesion

Associated with early p53 mutations and very aggressive behavior, invading myometrium. This is the one which is papillary-serous (psammoma bodies)

Other 80% is endometrioid (arising from hyperplasia in younger women)

65
Q

What type of ovarian cancer arises in the setting of endometrial cancer and are they related?

A

Ovarian endometrioid carcinoma
-> often arises in the setting of endometriosis, but the uterine endometrial cancer is independent (not a metastasis of the same tumor)

66
Q

How does hypothyroidism cause secondary lipoproteinemia? Why is this clinically relevant?

A
  1. Low BMR slows LPL activity
  2. LDL levels increased due to lack of T4 stimulation of SREBP2
    - > SREBP upregulates LDL receptors and cholesterol synthesis
    - > Explains why T4 is also needed to stimulate HMG-CoA reductase

Relevant because hyperlipidemia responds very well to T4 replacement therapy -> should be screening for hypothyroidism especially in young females with dyslipidemia

-> hyperthyroidism actually causes HYPOcholesteremia

67
Q

What are two common places for myxedema to occur in hypothyroidism? Why does this occur?

A

Larynx - giving them a deepening of the voice
Tongue - macroglossia

Occurs due to deposition of GAGs

68
Q

What condition is associated with anti-signal recognition peptide and anti-helicase antibody?

A

Polymyositis, Dermatomyositis

anti-Jo-1 = anti histidyl tRNA synthetase
anti-SRP = anti signal recognition peptide
anti-Mi-2 = anti helicase
69
Q

What labs will be seen in hyper IgE syndrome?

A

Elevated IgE, decreased IFNy (impaired Th17 activation), increased eosinophils (correspondingly elevated allergic response)

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