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Question Log Flashcards

1
Q

Acute onset CVP elevation, together with HOTN and tachycardia, can occur with what conditions?

A

cardiac tamponade or tension pneumothorax

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2
Q

Acute onset HF following viral illness should make you think?

A

dilated cardiomyopathy caused by viral myocarditis, which manifests as LV/RV dilation, mitral/tricuspid regurg, inc. ESV/EDV in LV
*unless there’s a high systolic pressure gradient between LV and aorta, because then that suggests LV outflow obstruction

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3
Q

Acute transplant rejection time frame and histopathology

A

1-4wks post-transplant; dense lymphocytic infiltrate in the interstitium of the organ

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4
Q

Aldolase B is part of what pathway?

A

Fructose (and Sucrose which can become fructose); Fructose to F-1-P is by Fructokinase, then F-1-P to Glyceraldehyde or DHAP is by Aldolase B

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5
Q

Alveolar transmural pressure and Intrapleural pressure

A

ATP is always positive; at FRC the airway pressure is 0 and there’s no force for bringing air in or out; at FRC the chest wall tendency to open and the lung tendency to collapse results in intrapleural pressure being about -5 cmH2O

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6
Q

Anti-Smith Ab - what does the Smith protein do?

A

Ab associated with SLE; the Smith protein complexes with snRNA to form a spliceosome, which cuts out introns from mRNA before it leaves the nucleus

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7
Q

Aortic stenosis, Afib, and Pulmonary edema

A

AS –> LVH –> dependent on atrial strength to fill up LV

Afib –> less likely to fully fill LV –> blood backs up into lungs –> pulmonary edema

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8
Q

Bilirubin metabolism pathway

A

Heme –[Heme Oxygenase]–> Biliverdin (green) –[Biliverdin reductase]–> Unconj Bilirubin –[Glucoronyl transferase]–> Conj bilirubin (liver) –[bacterial dehydrogenase]–> Urobilinogen (gut) –> Stercobilin –> brown color to feces

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9
Q

Bleeding from the nipple, think -

A

intraductal papilloma

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10
Q

Calculating resistance in parallel circuits

A

1/Rt = 1/R1 + 1/R2 + … 1/Rn

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11
Q

Can histamine antagonists be used in asthma?

A

Histamine antagonists are ineffective in asthma

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12
Q

Causes of dilated cardiomyopathy

A

Coxsackie B viral myocarditis, peripartum, alcoholism, thiamine def/wet beriberi, cardiotoxic drugs, chronic SVT

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13
Q

Causes of polyhydramnios

A

“decreased swallowing: esophageal/duodenal obstruction, intestinal atresia, or anencephaly
increased fetal CO: fetomaternal hemorrhage, Parvo infxn, alloimmunization”

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14
Q

CCBs’ effect on pacemaker cells vs. cardiac myoctes

A

“PM cells: will decrease/slow the Ca channel opening and thus Ca deolarization; this decreases the rate of firing of the SA and AV nodes
Myocytes: will decrease the opening of Ca channels, decrease the IC [Ca], and thereby reduced the excitation-contraction coupling”

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15
Q

Cells of bronchial epithelium

A

distal to terminal bronchioles = MPs; proximal is all lined with ciliated epithelium

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16
Q

Characteristics of mesothelioma

A

epithelioid neoplasm of the serosa, joined by desmosomes and have abundant tonofilaments with long slender microvilli; hemorrhagic pleural effusions are frequent and on CXR will see nodular or smooth pleural thickening

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17
Q

Cherry-red macula - ddx?

A

Hyphenated: Niemann-Pick (HSM; foam cells) and Tay-Sachs (tay-six; NO HSM; onion skin lysosome)

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18
Q

Clinical Triad: acute neuro abnormalities, hypoxia, and petechial rash on chest (following long bone fracture/surgery)

A

fat embolism to lungs

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19
Q

Common cause of pigmented stones

A

excretion of large amounts of conjugated bilirubin into bile, which is then deconjugated by beta-glucuronidase, causes pigmented stones; large amounts of bilirubin may result from chronic hemolysis, and lots of deconjugation (making it available for stones) is done by beta-glucuronidases which often come from bacteria and HCs injured in infection

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20
Q

COPD causes increase or decrease in FRC/TRV?

A

increase - because air is trapped

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21
Q

Cystic fibrosis - effects on pancreas and absorption

A

pancreas is damaged in CF, so ADEK are less absorbed; avitaminosis A is most likely to contribute to squamous metaplasia of the exocrine ducts in pancreas

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22
Q

DDx for painful thyroid nodules

A

De Quervain granulomatous thyroiditis - follows infection, self-limited, may start as hyperthyroid but ends up hypothyroid; will see early inflammation but the main thing is granulomas

Medullary thyroid carcinoma may also present as neck pain; pain here is more likely than in papillary thyroid carcinoma

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23
Q

Describe Myeloma cast nephropathy

A

when a pt has MM, there’s an overproduction of Bence Jones proteins (light chains) which are filtered by the glomerulus then reabsorbed in the tubule, but when it reaches limit for reabsorption the light chains are stuck in the tubule and end up forming casts with Tamm Horsfall proteins; when peed out these casts stain intensely pink (eosinophilic)
*Not to be confused with eosinophils in the urine (drug-induced interstitial nephritis)

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24
Q

Describe the shape and pH of the 4 types of kidney stones

A
  1. Ca oxalate - acidic pH, square envelopes (if Ca phosphate then basic pH)
  2. AMP - basic pH, coffin lids, from infxn with urease+ bugs (staghorn in adults)
  3. Uric acid - acidic pH, rhomboid or rosettes (radiolucent - unique)
  4. Cystine (aa) - acidic pH, hexagonal (staghorns in kids)
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25
Q

Differentiating between coarctation of the aorta and PDA?

A

coarctation will present with BP discrepancy, PDA will present with distal extremity cyanosis

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26
Q

DNA polymerase III has what activity? DNA pol I has what activity?

A

“Pol III: 5’–>3’ synthesis; 3’–>5’ exonuclease

Pol I: same as pol III but also removes RNA primer and replaces with DNA”

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27
Q

Does Cushing’s/excess ACTH cause hypertrophy or hyperplasia of (what level of the adrenal cortex)?

A

Hyperplasia of the fasciculata and reticularis (can be diffuse or nodular)

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28
Q

Doxorubicin AE on heart?

A

dose-dependent cardiotoxicity that produces dilated cardiomyopathy

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29
Q

Eccentric vs Concentric LVH

A

both are types of hypertrophy in response to an increased load; concentric is when the muscular wall gets bigger and thicker in order to pump against inc. afterload (like Aortic stenosis); eccentric is when the ventricle gets bigger and dilated in order to deal with the increased preload (like aortic regurgitation)

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30
Q

Effect of sex steroids on bone growth

A

Initially increase linear growth; also encourage closure of the epiphyseal growth plates

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31
Q

Effects of insulin

A

“promotes synthesis of TGs, glycogen, nucleic acids, and proteins
inhibits gluconeogenesis and glycogenolysis”

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32
Q

Explain endothelium-dependent vasodilation

A

“1. stimulus (including ACh, bradykinin, shear stress, substance P, and serotonin) induces rise of IC Ca

  1. inc. Ca induces ENOS which converts Arginine + O2 –> NO + citrulline
  2. NO diffuses over to smooth muscle where it stimulates GC
  3. active GC converts GTP to cGMP which activates pKG which reduces IC Ca and causes relaxation of the smooth muscle”
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33
Q

Explain hormones involved in anovulatory cycles

A

without ovulation there’s no progesterone, there’s just a cyclical rise/fall in estrogen; this means that the endometrium is perpetually proliferating, and bleeds whenever it become unstable and outgrows its own blood supply, instead of on a regular cycle. Results in irregular/longer menses.

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34
Q

Fabry’s Disease

A

XLR deficiency of alpha-galactosidase A; ceremide trihexosidase accumulates; angiokeratomas, peripheral neuropthy, hypohydrosis, and eventually renal failure; differentiate from Krabbe by the angiokeratomas

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35
Q

Factors that make a LVOT murmur louder

A

“decreasing the preload or afterload - this decreases the size of the LV and brings the mitral and aortic valves closer which is part of the LVOT obstruction; this is what causes SCD in pts with HCM
*Anything that increases preload or afterload - like squatting, passive leg raise, or sustained hand grip - would decrease murmur intensity”

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36
Q

Fate of K+ in the renal tubules

A

All of it is filtered; 65% reabsorbed in the PCT; 35% reabsorbed in the TAL (NaKCC); DCT/CD regulates final concentration of K - if low then it will reabsorb, if normal/high it will secrete K+

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37
Q

For a patient in afib, what is the determining factor for ventricular rate?

A

AV node refractory period - this is the RLS since they will get signals and pass them on, it just won’t be organized signals, so they pass them on as fast as they can
bronchogenic carcinoma is #1 malignancy and

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38
Q

for asbestos exposure:

A

mesothelioma is rare; can also see pleural plaques, pulmonary fibrosis, and asbestos bodies

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39
Q

Gallstones in pregnancy

A

high estrogen causes upregulation of HMG-CoA reductase and thus the bile is hypersaturated with cholesterol, plus progesterone causes gallbladder hypomotility – resulting in cholesterol stone formation; can have same effect from OCPs

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40
Q

Gaucher’s disease

A

deficiency of glucocerebrosidase; glucocerebroside accumulates; triad = HSM, avascular necrosis of femur (severe hip/knee pain, aka Legg-Calve-Perthes disease) and osteoporosis, specific finding of MPs that look like crumpled tissue paper (Gaucher cell), yellow-brown skin pigmentation (non-specific); “young patient with easy bruising and anemia/pancytopenia, joint pain, MASSIVE liver and/or spleen, diffuse petechiae”

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41
Q

von Gierke disease

A

GSD type I - missing G-6-phosphatase, can’t get glucose OUT of the liver

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42
Q

Respiratory/metabolic changes in high alititude

A

high altitude –> hyperventilation –> blow off CO2 –> respiratory alkalosis –> kidneys secrete bicarb

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43
Q

Gout presents as what type of joint reaction?

A

acute inflammatory process; therefore treat with NSAIDs aimed at reducing PGs/NTs or Colchicine which inhibits NT activation and migration

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44
Q

Hepatosplenomegaly - ddx?

A

Gaucher (hip/knee pain), Niemann-Pick (cherry red macula), Hurler’s (gargoylism, cloudy corneas) and Hunter’s (gargolyism + aggression, no cloudy corneas)

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45
Q

Hgb subunits? Myoglobin? O2 dissociation curve of each

A

Hbg subunits = 2 alpha and 2 beta, each has a heme group; Myoglobin = monomer, 1 heme (so basically just like 1 beta subunit of Hgb); O2 dissociation curve is sigmoidal for Hgb because of the multi-heme interactions while it’s straight up and asymptote near 100% for myoglobin/monomer

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46
Q

High estrogen comes from where and causes what?

A

“thickened endometrium” - think high estrogen; if ovarian mass too - granulosa cell tumor; then look for Call-Exner bodies (description: cuboidal granulosa cells in a rosette pattern with coffee bean nuclei)

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47
Q

Histological presentation of kidneys following RAS

A

the one with the stenotic artery will be smaller and the other one will be bigger due to compensatory hypertrophy

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48
Q

Holosystolic murmur that increases in intensity during inspiration

A

tricuspid regurgitation

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49
Q

How are parasites killed by eosinophils?

A

the parasites are first covered by Abs; the eo’s then bind those Abs with their Fc receptors and that causes them to degranulate their MBP; this is a form of ADCC

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50
Q

How do you get neurological sx from hyperventilation?

A

tachypnea –> hypocapnia –> vasoconstriction (has to do with pH) –> decreased ICP
hypocapnia during hyperventilation causes neuro sx, it also causes vasoconstriction (related? dunno)

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51
Q

How does CHF affect lungs?

A

well of course you get a transudate into the interstitium, but the real effect of this is that the lung compliance is decreased because there’s distortion and swelling in the tissue and it’s harder to open the lung; creates the same net effect as pulmonary fibrosis and insufficient surfactant

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52
Q

How does depolarization happen in the 3 major muscle types?

A

“Cardiac: depolarization opens L-type CaCh, influx opens the RyR2 receptor in the SR which releases more Ca to bind troponin to let actin and myosin interact
Smooth: same as cardiac except instead of Ca binding troponin, Ca binds calmodulin and this lets actin and myosin interact
Skeletal: L-type CaCh interact directly with the RyR1 receptors and don’t need an influx of Ca to open it, then Ca binds troponin and actin/myosin interact”

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53
Q

How does GH make someone taller?

A

It acts to increase the IGF being released from the liver, which has the direct growth effects

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54
Q

How does PAH get cleared?

A

majority is filtered in glomerulus but then a lot is secreted by the PCT; none is reabsorbed

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55
Q

How does silicosis affect MPs?

A

damages them; thought that the MP eat the silicon fibers and break

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56
Q

How long does it take after birth for PVR to decline enough to hear a left-to-right shunt murmur?

A

4-10d

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57
Q

How to calculate the RBF using PAH?

A

RBF = PAH clearance = (Urine PAH * Urine Flow rate) / [PAH in plasma]
–> be careful if they give you a serum concentration; then you have to convert: Plasma = 1 - Hct

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58
Q

How to differentiate an Granulosa cell tumor and a Sertoli-Leydig cell tumor?

A

GCT –> Estrogen which will produce ABNORMAL uterine bleeding 2/2 endometrial hyperplasia, and precocious puberty
SLCT –> Testosterone which will produce virilization meaning AMENORRHEA, deep voice, hirsutism, clitoromegaly

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59
Q

How to differentiate dermatitis herpetiformis from atopic dermatitis that is triggered with eating certain foods?

A

DH is going to occur in 4-5th decade; AD typically presents in infants and usually before age 5

DH usually affects the buttocks/extensor surfaces; AD in infants will involve scalp/extensor surfaces but spare the diaper area, then in older kids will affect the flexor surfaces

DH is associated with Celiac disease, which also has LC infiltration, crypt hyperplasia (not crypt abscesses - that’s UC), and loss of villi which would make for malabsorption/steatorrhea.
AD is associated with asthma and allergic rhinitis = allergic triad.

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60
Q

How to recognize a pulmonary abscess

A

if the abscess communicates with an air passage there will be partial drainage enough for an air cavity to form which can be seen on CXR; this abscess is forming because of release of lysosomal enzymes from the dying NTs/MPs; there can also be an air-fluid level on imaging.
Symptoms = night sweats, fever, weight loss, and productive cough with foul-smelling sputum

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61
Q

Hypocapnia implies

A

alveolar hypoventilation (assuming constant rate of CO2 production)

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62
Q

In a patient with dementia, prior stroke, and PNA, what is the most likely cause of the PNA?

A

aspiration (can lead to septic shock, lactic acidosis)

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63
Q

Incontinence and DM1

A

think diabetic autonomic neruopathy–affecting detrusor muscle; also don’t feel the urge and can’t empty completely, with difficulty starting/stopping

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64
Q

Ivabradine

A

selectively inhibits funny sodium channels in the SA node cells, thereby slowing HR; it’s the only drug that has NO effect on contractility or relaxation; used in treatment of HF (reduces the risk of hospitalization)

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65
Q

Kidney stones and Calcium levels

A 
#1 reason for kidney stones is hypercalciuria - makes sense because if you have too much Calcium then your body tries to dump it in the kidneys, instead of leaving it in circulation
for that reason there's normal serum calcium levels
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66
Q

Know what direction glycolysis goes when you have high Fructose

A

down glycolytic pathway

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67
Q

Law of Conservation of Mass - as applied to a blood vessel that gets smaller

A 
Qin = Qout --> V1*A1 = V2*A2
Q = flow; V = velocity; A = diameter of vessel
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68
Q

Mainstem bronchus lesion

A

from obstruction of the bronchus you get air trapped in the lung, then it all gets absorbed into the blood; when no more air in the alveoli –> atelectasis; trachea deviates toward side of lesion because of lower pressure when lung collapses

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69
Q

Major basic protein is for

A

for parasites, as it’s “anti-helminth”

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70
Q

Man with testicular tumor and hyperthyroidism - likely diagnosis?

A

Choriocarcinoma - because this tumor secretes hCG, the alpha subunit of which is similar between hCG, TSH, FSH, and LH (may also see gynecomastia)

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71
Q

Midline episiotomy will involve what structures?

A

vaginal lining/mucosa and perineal body

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72
Q

MOA of the CFTR

A

CFTR uses ATP hydrolysis

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73
Q

most common benign pulmonary lung tumor:

A

hamartoma - “popcorn calcifications” with islands of mature hyaline cartilage

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74
Q

Most frequent mechanism of SCD following MI/coronary artery occlusion

A

V-fib

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75
Q

Neurophysins

A

carrier proteins for ADH/oxytocin to move them down to the nerve terminal for release in posterior pituitary

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76
Q

Normal Pressures in cardiac cath

A 
SVC/RA: 1-6mmHg
RV: systolic is 15-30mmHg
PA: diastolic is 6-12mmHg
Pulm wedge: 6-12mmHg (~PA diastolic) 
LA: 10mmHg (higher in mitral regurg)
LV: ~120mmHg (same as aorta)
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77
Q

Pancoast tumor is also called:

A

Superior Sulcus tumor

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78
Q

Pancreatitis is a major risk factor for what lung disease?

A

ARDS

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79
Q

What size particle are dealt with by mucociliary transport in the respiratory tract?

A

2.5-10 micrometers = mucociliary transport

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80
Q

Pentad of sx makes you think:

fever, neuro sx, RF, anemia, thrombocytopenia in the setting of GI illness

A

TTP-HUS or another thrombotic microangiopathy

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81
Q

Peripheral neuropathy (LSD) - ddx?

A

“EE”: Fabry (angiokeratoma) and Krabbe (optic atrophy)

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82
Q

Phenylalanine metabolism pathway

A

Phenylalanine –> Tyrosine* –> DOPA (–>melanin)
Can’t convert to Tyrosine = PKU
Can’t convert to DOPA = Albinism

*Tyrosine –> Homogentisate ->->-> Fumarate
Can’t convert Homogentisate = Alkpatonuria

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83
Q

Problems limited to the right heart - think

A

carcinoid syndrome (and most commonly, serotonin/bradykinin)

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84
Q

PRPP is an enzyme where?

A

in the purine/pyrimidine synthesis pathway; without it you get gout (deposition of needle-shaped, negatively birefringent crystals in joints)

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85
Q

Ras-Raf-Mek-Erk-TF - what activates Ras?

A

Ras is a G-protein that gets activated when it binds GTP; it’s inactivated form is when GTP is cleaved into GDP and it hangs out like that; a mutated Ras may never again cleave GTP into GDP and thus would be constitutively active always, leading to continuous proliferation/cancer

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86
Q

Rate of Inulin clearance best approximates ?

A

GFR

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87
Q

Ratio of phosphatidylcholine (aka lecithin) to sphingomyelin in amiotic fluid?

A

approximately 1:1 until week 35 (3rd trimester) when lecithin will rise sharply as fetal lungs start to produce surfactant; will rise to 2:1 or higher

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88
Q

Reactive arthritis - how to recognize it?

A

since it’s a seronegative spondyloarthropathy, look for a single involved joint about 1-4wks following an infection; may also have the other symptoms of conjunctivitis and urethritis; associated strongly with HLA-B27, but not serum markers
*Reactive arthritis may also involved sacroiliitis, dactylitis, hyperkeratotic vesicles on palms/soles, dermatitis of glans penis (circinate balanitis), and oral ulcers

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89
Q

Relationship between Ca and granulomatous disease

A

activated MPs (in granulomas) can express 1-alpha-dehydroxylase which will activate Vit D and increase Ca, independent of PTH

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90
Q

Relationship between PTH, Vit D, Ca, PO4, and Mg

A

low serum Ca or Mg will inc. PTH; really high Mg will dec. PTH; when PTH is secreted it will tell kidney to retain Ca and dump PO4 because PO4 likes to bind up free Ca; diarrhea will cause low Mg

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91
Q

Retinopathy of prematurity

A

when a baby is born premature and they have hypoplastic lungs they will be treated with O2 and/or CPAP; the hypoxia however will induce angiogenic factors in the retina, which start neovascularization when there is sufficient O2 (like when the nurse gives it) and all the neovascularization will increase the risk of retinal hemorrhage/detachment, hence retinopathy (this is a major cause of blindness in developed countries)

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92
Q

Roles of HGPRT and PRPP in purine synthesis

A

HGPRT is purine salvage and PRPP is de novo synthesis; so in the case of Lesch-Nyhan when you’re missing HGPRT you can’t keep up with all the purines that need recycling and they get shunted/stuck as Hypoxanthine/Guanine, Xanthine, and Uric acid

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93
Q

Signs of normal aging in the heart

A

sigmoid shaped ventricular septum, increased interstitial collagen/CT, and accumulation of brown cytoplasmic granules containing lipofuscin (wear and tear pigment)

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94
Q

Sorbitol pathway

A

“Glucose –> Sorbitol –> Fructose

Aldose reductase / Sorbitol dehydrogenase”

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95
Q

Theca cells make?

Granulosa cells make?

A

TAGE
Theca –> Androgens
Granulosa –> Estrogen

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96
Q

Thionamide induced agranulocytosis

A

both methimazole and PTU can produce agranulocytosis; so if a patient has fever and sore throat get a WBC with differential to rule out agranulocytosis and probably stop the drug asap; this side effect makes radioactive iodine the preferred treatment for hyperthyroidism (including Grave’s disease)

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97
Q

Thoracic outlet syndrome

A

presents as numbness, tingling, weakness, and maybe swelling (if vein involved) of the upper extremity; outlet is most commonly obstructed at the scalene triangle (formed by ant and middle scalenes and the first rib)

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98
Q

Thymomas or thymic hyperplasia is associated with what disease of bone marrow?

A

pure red cell aplasia - the thymus makes T cells that then develop a destructive affinity for RBCs only (via IgG or CTLs); this could also be due to Parvovirus B19 infection

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99
Q

Total PVR is lowest at ?

A

lowest = FRC; at max inspiration the alveoli are full of gas and put pressure on the capillaries; at max expiration there’s lots of intrathoracic pressure on the capillaries; so happy medium is where you’re not breathing in or out

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100
Q

Transient myocardial ischemia causes cells to increase in size. What happens?

A

decreased O2 causes cell to switch to anaerobic metabolism, but can’t make as much ATP so the Na/K ATPase in the membrane fails, as well as the Ca-ATPase in the mitochondrial membrane; this build up of IC Na and Ca is bad for the cell and causes swelling - the primary cause of the increased size
Failure of the SR to sequester Ca results in decreased contractility of the muscle

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101
Q

What aa’s anchor a protein into the cell membrane?

A

nonpolar, hydrophobic aa’s like: ala, val, leu, phe, tryp, met, pro, gly

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102
Q

What are the 2 ways to represent CO?

A

CO = SV * HR = O2 consumption / arteriovenous O2 difference

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103
Q

What are the cardinal veins?

A

in utero they are the veins that eventually become the systemic veins; in contrast to the umbilical and vitelline veins which degenerate and form the portal system, respectively

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104
Q

What are the normal partial pressures for O2 and CO2?

A

Normal PaO2=75-105, PAO2=105

Normal PaCO2=33-45, PACO2=40

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105
Q

What are the vascular changes that occur in malignant HTN? DM? atherosclerosis?

A
  1. malignant HTN - onion skinning/concentric hypertrophy of small vessels
  2. DM - hyaline arteriosclerosis/homogenous acellular pink material; stains pink with PAS stain
  3. atherosclerosis - lipid-filled intimal plaque covered by fibrous cap (ECM and fibrous cap made by VSMCs)
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106
Q

What cell types line the female reproductive tract?

A

Ovary - cuboidal; Fallopian tubes and Uterus - simple columnar; Cervix - simple columnar to stratified squamous (NK); Vagina - stratified squamous (NK)

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107
Q

What cofactor is most often required for transfer of groups between/to amino acids?

A

B6 - required for decarboxylation and transamination of amino acids, as well as for gluconeogenesis

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108
Q

What do hemosiderin laden MPs look like and how do they stain?

A

golden cytoplasmic granules within MPs that stain blue with Prussian blue (stains the iron in the blood)

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109
Q

What do the enzymes PNMT, COMT, and MAO do?

A

“PNMT: converts NE to Epi
COMT: breaks down NE –> normetanephrine; Epi –> metanephrine
MAO: breaks down NMN/MN into vanillylmandelic acid (VMA)”

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110
Q

What do the Purkinje PM cells do?

A

they are ectopic PM cells that can assume pacemaker activity during bradycardia

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111
Q

What does Buerger disease look like?

A

they’ll tell you it’s an Asian male (young) who has something to do with smoking/tobacco - could be hypersensitivity rxn to tobacco component; and they have vascular insufficiency in the extremities, and this segmental vasculitis is unique in that it extends into contiguous veins and nerves

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112
Q

What does left dominant circulation mean?

A

That the PDA is fed primarily by the Left coronary circulation, specifically the L circumflex artery.
The PDA also gives rise to the AV nodal artery; so whichever coronary is dominant, that the one that feeds the AV node.

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113
Q

What factors affect airway resistance?

A

airway resistance is increased by smaller diameter and turbulent airflow (in larger diameter); it’s decreased by total cross sectional area which is maximal in small bronchi and beyond

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114
Q

What form of O2 in blood doesn’t change?

A

partial pressure of dissolved O2

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115
Q

What happens to C peptide?

A

it gets cleaved from the proinsulin molecule by beta-peptidases but is secreted alongside, so it ends up in circulation

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116
Q

What happens to the thyroid pool when you take Estrogen/Progesterone?

A

estrogen increases the amount of TBG, so more thyroid is bound up and less free T3/T4 - this feeds back to pituitary to increase TSH; TH then saturates the TBG and repletes the free T3/T4; so net effect is that the total TH goes up while free T3/T4 stays the same

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117
Q

What is a glomangioma and where is it found?

A

a tumor of the modified smooth muscle cells of a glomus body, which is a small encapsulated neurovascular organ found in the dermis of the nail bed, finger/toe pads, and ear; the glomus body functions to sense the temp and dilate or constrict to let heat out/in

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118
Q

What is PFK1 and PFK2 and when are they active?

A

PFK1 converts F-6-P to F-1,6-BP in glycolysis.
PFK2 converts F-6-P to F-2,6-BP in the side path that is going to sense whether you need to run glycolysis or not.

Fed state: inc. F-2,6-BP will push PFK1 to run glycolysis.
Fasting state: Glucagon has inc. cAMP/pKA which drives PFK2 backwards to make more F-6-P to turn into glucose (MAIN GOAL = GLUC)

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119
Q

What do Homeobox genes code for?

A

transcription factors that alter expression of genes that will result in the cranio-caudal segmentation of the embryo; mutations in these genes will result in improperly placed organs and limbs and skeletal abnormalities

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120
Q

Amitryptiline

A

a TCA with strong anticholinergic properties

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121
Q

Clinical features of Vitamin A deficiency

A

night blindness, coarse/itchy skin, eye dryness +/- corneal ulceration, growth retardation, immune impairment

122
Q

What does antiphospholipid antibody syndrome look like?

A

venous/arterial thromboembolism, miscarriages, premature birth 2/2 placental insufficiency or preeclampsia, paradoxical prolonged aPTT that doesn’t reverse, and false-positive RPR/VDRL
PLUS
symptoms of lupus: glomerulonephritis, skin photosensitivity, and arthralgias

123
Q

What does the 95% confidence interval indicate?

A

that is the value falls in that range, you can be 95% sure it’s statistically significant

Calculated: Mean +/- 1.96*SD

To account for variability when not measuring the entire population, incorporate standard error: SE = SD/(square root of n)

So when trying to find the CI of the mean of a population sample, calculate:
CI = mean +/- 1.96SE
CI = mean +/- 1.96(SD/sqrt[n])

124
Q

How is copper absorbed, carried, and excreted?

A

absorbed: stomach and duodenum
carried: ceruloplasmin
excreted: hepatic excretion via bile/stool; 5-15% via renal but that’s minority

125
Q

What do neurons look like 12-24hr post-ischemic stroke?

A

“red neurons” - intensely eosinophilic cytoplasm, loss of Nissl substance, and pyknotic nuclei.
Beyond 2 wks there’s glial scar formation, >1mo there’s a cystic area surrounded by dense glial fibers

126
Q

“glycoprotein” in the context of cancer cells - think

A

P-glycoprotein, the ATP-dependent efflux pump that makes the cells resistant to chemo drugs (MDR1 gene)

127
Q

Redistribution of thiopental takes it where?

A

mostly to skeletal muscle and adipose tissue, but also to other organs.
it’s fat-soluble

128
Q

Aortic arch derivatives

A 
1 - maxillary artery (portion)
2 - hyoid and stapedial arteries
3 - CCA, ICA
4 - L: aortic arch; R: prox R subclavian
5 - nothing
6 - prox PA, ductus art
129
Q

Elevated MMA in urine - ddx?

A

MMA –> MM-CoA –> Succinyl-CoA –> TCA cycle
= B12 deficiency - would lead to inability to convert MMA to Methylmalonyl-coA, from MMA build-up get impaired myelin synthesis

OCFA/AA –> Propionyl-CoA –> MM-CoA –> Succinyl-CoA –> TCA cycle
= Congenital MM-CoA mutase deficiency - would lead to inability to convert MM-CoA to succinyl-CoA meaning build up of propionyl-CoA (from OCFA, threonine, methionine, isoleucine, and valine) which causes elevated MMA, PPA, and ketones in urine; plus hypoglycemia, metabolic acidosis (from ketone production), and hyperammonemia

130
Q

Common MOA of drug infusion followed by diffuse pruritis

A

medication-induced (IgE-independent) mast cell degranulation

–> opioids, radiocontrast agents, and some abx (e.g., vanc)

131
Q

Anti-mitochondrial antibody, association with Sjörgen syndrome, and liver issues - condition? histology?

A

Condition: most likely primary biliary cirrhosis (PBC)
Histology: destruction of small/mid intrahepatic bile ducts with lymphocytic infiltrate, results in cholestasis; may also see Mallory-Denk bodies
Findings: fatigue, itching (esp. at night), hepatomegaly, xanthomas, jaundice; elevated serum Alk-Phos, IgM, and cholesterol; then confirm dx with anti-Mi Abs

132
Q

Histopathology of acetaminophen overdose

A

central lobar necrosis, can extend to entire lobule; liver failure

133
Q

Alcoholic hepatitis - histopathology

A

cellular swelling, necrosis, Mallory-Denk bodies (damaged intermediate filaments within HCs), NT infiltration, fibrosis

134
Q

Vasopressin acts to increase reabsorption of what in the kidney?

A

water and urea

135
Q

Friederich ataxia

A

(AR) GAA trinucleotide repeats in Chr 9 makes for mutated frataxin

  • means problems with Fe and free radical formation in mitochondria
  • results in degeneration of spinocerebellar and lateral corticospinal tracts –> gait ataxia, spastic muscle weakness
  • presents as young person with kyphoscoliosis, high plantar arch (pes cavus), HCM/CHF
136
Q

Pathogens most often responsible for bacterial PNA following influenza infxn

A
  1. S. pneumo
  2. S. aureus
  3. H. flu
137
Q

Baclofen

A

GABA-A agonist

useful for spasticity 2/2 brain/spinal cord disease such as MS

138
Q

Timeline for brain cell changes following ischemic stroke

A 
0-48hr = red neurons
3-5d = NTs then microglia move in and phagocytose the broken down cells
then = cystic space replaces area of necrosis; astrocytes forms a glial scar
139
Q

MOA of ANP/BNP

A

binds ANP receptor which stimulates GC, increases cGMP, and causes vasodilation

140
Q

Histone proteins

A

H1 = outside the core

H2A/B, H3, H4 = make up the core

141
Q

How to differentiate T-ALL from B-ALL in a kid with leukemia?

A

First of all - general sx of ALL include fever, fatigue, pallor, petechiae, and bleeding

T-ALL more likely to present with mediastinal mass that causes SVC syndrome, compress the esophagus leading to dysphagia, or compress the trachea leading to dyspnea

Then on staining both will have TdT+ (indicated lymphoid lineage) and T cells will have CD2/3/4/5/7/8 and B cells will have CD10/19/20

142
Q 
Effects of prolonged glucocorticoid use on:
skeletal muscle
adrenals
bone
liver
adipose
skin
immune system
A

skeletal muscle - atrophy
adrenals - atrophy
bone - osteoporosis
liver - increased gluconeogenesis/glycogenesis (increased protein synthesis to keep up with demand)
adipose - fat redistribution, lipolysis
skin - striae, thinning, impaired wound healing
immune system - suppression, T cell apoptosis

143
Q

Antibodies in erythroblastosis fetalis/hemolytic disease of the newborn (HDN)

A

Mother O, will have IgG anti-A/B
Mother A/B, will have IgM anti-B/A
*If the mother is blood type A or B - the abs will be IgM, and therefore won’t cause problems because they can’t cross the placenta

144
Q

Most common site for compartment syndrome in the leg

A

Anterior compartment - includes the foot extensor muscles (dorsiflexion), deep peroneal nerve, and anterior tibial artery and veins

145
Q

Fenoldopam

A 
short-acting D1R agonist
rapidly vasodilates (inc. cAMP), especially renal arterioles --> inc. renal perfusion and natriuresis
146
Q

What med is best to reduce airway inflammation in asthma?

A

glucocorticoids:

  • inhaled for long-term use
  • systemic for acute exacerbations

*LTs (e.g. montelukast) are also used long-term to reduce airway inflammation but they are not nearly as efficacious nor as anti-inflammatory as steroids

147
Q

What is the significance of ether and viruses?

A

ether (and other organic solvents) can inactivate a lipid bilayer; therefore enveloped viruses can be inactivated by ether; this is because the bilayer is derived from the last cell it left and is needed for entry into the next cell

148
Q

Inhibin

A

hormone secreted by Sertoli cells in the seminiferous tubules responsible for negative feedback to hypothalamus to say, we have enough FSH
Look out for low inhibin when the testes are undescended as the higher temps will damage the seminif. tubules, and no inhibin means really high FSH that falls on nonfunctional sertoli cells
*also inc. risk of cancer in undescended testes

149
Q

What spinal cord levels do these reflexes come from:
Biceps
Bracioradialis
Triceps

A

Biceps - C5-6
Brachioradialis - C5-6
Triceps - C7-8

150
Q

Phenylephrine

A

administered for pupil dilation -

selective a1 agonist for the pupillary dilator muscle (causes contraction which results in pupil dilation)

151
Q

Myopathy and statins

A
  • statins, which inhibit HMG-CoA reductase, has main side effects of myopathy and hepatitis
  • can see a myopathy seen by increased serum CK levels and also muscle weakness relieved by stopping the statin
  • the myopathy is worsened when fibrates (especially gemfibrozil) are taken concurrently because they impair hepatic clearance of the statins, allowing them to achieve higher serum levels
152
Q

Categories of hypoglycemic symptoms

A
  1. Neurogenic - SNS in control: releases NE/Epi and causing tremulousness, anxiety, palpitations; also releases ACh causing sweating, hunger, paresthesias
  2. Neuroglycopenic - behavior changes, confusion, visual disturbances, stupor, and seizures
153
Q

3 treatment options for C. diff and their indications

A
  1. Metronidazole (IV) - the most systemic absorption; used for mild to moderate cases, 1st and 2nd infections – but not subsequent
  2. Vancomycin (PO) - SEVERE infection, first or recurrent; is only bacteriostatic at employed doses
  3. Fidoxamicin (PO) - oral drug with bacteriocidal activity, minimal systemic absorption, and a narrow spectrum (hits on C. diff only); best choice for multiple recurrent infections because it has a better cure rate than the others
154
Q

Deficiency of what enzyme would cause maternal virilization in pregnancy with a female fetus?

A

aromatase deficiency - will give high androgen and low estrogen levels, the excess androgens spill over to mom

Normally aromatase will convert androstenedione to estrone, and testosterone to estradiol
Majority should happen in the placenta, thus if it’s broken it’s close to mom in the placenta

155
Q

What nerve is most commonly injured at the lateral head of the tibia and what symptoms would it cause?

A

Common peroneal nerve (which splits into deep and superficial peroneal nerves)
Would cause foot drop and inability to extend the toes upward (DPN); also inability to evert the foot (SPN) with loss of sensation over the foot dorsum and lateral leg (SPN)

156
Q

Takes a long time to slough umbilical cord - what’s the problem?

A

Leukocyte adhesion deficiency (LAD) - low expression of integrins from absence of CD18 (AR)

157
Q

Candida spreads and the cells that contain them

A
  1. Superficial - T cells
  2. Hematogenous/Disseminated - NTs
    * So someone with HIV will probably get cutaneous candida, but won’t get disseminated infection unless they have a neutropenia (as in hematologic malignancy/chemo)
158
Q

Surface marker for monocyte/MP lineage

A

CD14

159
Q

Target(s) of GVHD

A

a particular organ may be the target but the most common are skin, GI, and liver
Look for patient with recent transplant and within a week or two gets a diffuse rash and N/V/D, ulcerations of intestinal mucosa

160
Q

Predispositions to developing chronic giardiasis

A
  1. IgA deficiency
  2. X-linked agammaglobulinemia (BTK)
  3. CVID
161
Q

Acute respiratory distress syndrome

A

“Diffuse Alveolar Damage”
Alveolar walls get proteinaceous fluid leakage which becomes hyaline membranes.
This causes decreased gas exchange/hypoxemia/cyanosis, as well as diffuse lung collapse because the hyaline membranes are “sticky”.
Etiology is many, all converge on activating NTs which let out proteases and free-rads, these factors damage type I AND II pneumocytes - makes it harder to regenerate lung tissue (Type 2 PC’s are stem cells) and get interstitial fibrosis instead.

162
Q

Neonatal respiratory distress syndrome

A
  • lecithin (phosphatidylcholine) increases after week 36, when it’s 2x sphingomyelin then the lungs are mature
  • the following increases risk of NRDS: maternal diabetes (baby pancreas produces lots of insulin to keep up; insulin inhibits surfactant production); C-section (no stress –> cortisol –> no lung opening)
  • placing baby on 100% O2 will create lots of free radicals, can damage lungs and retina
163
Q

Major inducers of CYP3A4

A 
CROPP GGGAS:
Carbamazepine
Rifampin
OCPs
Phenobarbital
Phenytoin
Griseofulvin
Ginseng
Green vegetables
Alcohol, chronic use
St. John's Wort

–> decrease Warfarin effect
Crop gas makes crops grow = inducers

164
Q

Major inhibitors of CYP3A4

A

Say No To CRACK AMIGGOSS:
SSRIs/Fluoxetine
NSAIDs/Acetaminophen
Thyroid hormone

Cimetidine
Ritonavir/Protease inhibitors
Amiodarone
Ciprofloxacin, Erythromycin/Abx
Ketoconazole/Azoles/Metronidazole
Acute Alcohol use
Macrolides
Isoniazid
Grapefruit/Cranberry juice
Gingko Biloba
Omeprazole
Sulfonamides

+Vit E
–> inc. Warfarin effect
“Say No” = inhibition

165
Q

Drugs that can cause QT Prolongation

A

“Some Risky Meds Can Prolong QT”
Sotolol, Risperidone, Macrolides, Chloroquinolone, Protease inhibitors, Quinidine, Thiazides
**Amiodarone can prolong the QT interval but it has little risk of becoming torsades

166
Q

Medications to avoid in pts with HCM

A

vasodilators and diuretics - because anything that decreases preload or afterload (ultimately decreasing the LV volume) will worsen the LVOT obstruction by allowing the LV to collapse

*HCM can cause chest pain by producing a sort of ischemia during exertion, whenever the preload or afterload decreases you get increased LVOT obstrucion and thus less coronary supply

167
Q

What kind of splitting do ASDs cause?

A

wide and fixed splitting of S2

because increased volume makes its way to the R heart with every contraction

168
Q

Pulsus paradoxus

A

A drop in SBP >10 on inspiration (normally increased)
Caused by diseases affecting R ventricle expansion into the pericardium, like cardiac tamponade.

During inspiration the R heart is super-filled and won’t normally compress the left ventricle, but if there’s something else pushing on it (like cardiac tamponade) then the only option is to decrease the size of the left ventricle, thereby decreasing outflow - hence drop in SBP.

In the absence of pericardial disease, the MCC is obstructive pulmonary disease (asthma/COPD exacerbation). Treat with bronchodilators - B2R agonists

169
Q

Lymph drainage - scrotum, testes, glans penis, posterior cutaneous calf

A

Superficial inguinal LNs drain nearly all cutaneous lymph from umbilicus and below, including external genitalia and anus, below dentate
*Exceptions = testis, glans penis, cutaneous post calf

Scrotum –> superficial inguinal LN
Testes –> para-aortic (RP) LNs
Glans penis, post cutaneous calf –> deep inguinal LNs

Superficial Inguinal LN –> Deep Inguinal LN

170
Q

Ureteral circulation

A

Proximal ureter - branches off renal artery
Middle ureter - gonadal artery
Distal ureter - common iliac artery, internal iliac artery, vesical artery

171
Q

Where is a transplanted kidney placed?

A

retroperitoneal in the right iliac fossa

172
Q

What organs are located retroperitoneally?

A 
SAD PUCKER
S - suprarenal glands
A - aorta/IVC
D - duodenum (except 1st part)
P - pancreas (except tail)
U - ureters
C - colon (asc/desc)
K - kidneys
E - esophagus
R - rectum
173
Q

What predisposes to drug-induced lupus?

A

slow-acetylators
Hydralazine, Isoniazid, Procainamide
Minocycline, TNF-alpha inhibitors

174
Q

Guillan-Barre syndrome - MOA

A

ascending weakness/paralysis following a URI (Campylobacter); an immune-mediated demyelination of spinal cord and peripheral nerves - get segmental demyelination on LM along with endoneural inflammatory infiltrate (LCs/MPs)

175
Q

HPV of head/neck likes to infect what locations?

A

like basal epithelial cells - so stratified squamous cells in the true vocal cords

176
Q

Most common congenital heart defect in Turner and Down’s syndrome

A

Turner - bicuspid aortic valve

Downs - no/bad AV valves, ASD, and VSD (endocardial cushion defects)

177
Q

MCC of IVH in pre-term infants?

A

Hemorrhage from germinal matrix (origin of migrating neurons)
Bleed will occur within 5d post-natal and appear as bulging fontanel, HOTN, decerebrate posturing, tonic-clonic seizures, irregular respirations, coma

*Pre term = before 32wks and/or

178
Q

MOA of bisphosphonates

A

Inhibition of mature osteoclast-mediated bone resorption

*Note the cells are already mature, the meds don’t inhibit maturation or anything

179
Q

Outcomes of HBV infection

A

Most resolve completely (>95%).
4-5% will become chronic, and only 20-50% of those will get cirrhosis, of those 10% will get HCC.
Fulminant hepatitis happens in

180
Q

Persistent lymphedema will increase the risk for

A

lymphangiosarcoma

181
Q

Cavernous hemangioma

A

benign neoplasm of endothelial cells of small blood vessels

  • MC benign tumor of the liver
  • in the brain they are usually in the parenchyma and can cause seizures
182
Q

MCC of ED

A

SSRIs (50% of pts on them have sexual dysfunction)
Atherosclerosis
?

183
Q

Antibodies against PRP is protective against what?

A

H. influenza (B)

184
Q

Treatment for peripheral artery disease

A
  1. platelet inhibitor
  2. arteriole dilator - need this to stop the claudication

Cilostazol - inhibits PDE, thereby inhibiting plt aggregation and causing vasodilation

185
Q

Most common catalase-positive organisms that afflict pts with CGD

A

Aspergillus, Burkholderia cepacia, Nocardia, Serratia marcescens, and S. aureus,

186
Q

Fifth disease - pathogenesis

A

Caused by Parvo B19 (ssDNA linear - the only one)
enters by respiratory droplets, causes congestion, HA, low-grade fever, then you get a lace-like, erythematous rash that starts as flushed cheeks then spreads down to include the trunk
The virus replicates in erythrocytes, and thereby can cause aplastic anemia in SCD

187
Q

How to treat widened QRS interval?

A

Sodium bicarbonate

Potential causes of prolonged QRS = something that binds Na channels and prevents the influx of sodium

  • Flecainide, Class IC anti-arrhythmic
  • TCA overdose, which blocks the fast sodium channels causing seizures, delirium, cardiac abnormalities, severe HOTN, and signs of ACh toxicity

NaHCO3 good for treating ventricular arrhythmias, basically by providing so much Na that some will leak in past the block.

188
Q

How to recognize a manic episode?

A

DIG FAST:
Distractibility, Impulsivity, Grandiosity, Flight of Ideas, Activity increase, Sleep decrease, Talkativeness

+/- delusions or hallucinations

–> Should make you think Bipolar I because depressive episodes are not needed for diagnosis

189
Q

Organ of Corti vs. Cochlear cupula

A

Organ of corti - the steroeciliated hair cells that transduces the sound from the vibrating tectorial membrane
Cochlear cupula - located at the apex of the cochlea, registers low-frequency sound

190
Q

Edema and hemorrhagic necrosis of the temporal lobe - infection?

A

HSV-1 encephalitis; results from oropharyngeal infection that spreads via olfactory tract, or latent viral infection in trigeminal ganglion

191
Q

Osteocytes connect to each other in lamellae by…?

A

gap junctions - so they can continue to communicate

192
Q

MCC of Turner syndrome

A

paternal non-disjunction in gametogenesis

193
Q

Fishy odor plus clue cells

A

Gardnerella - Clindamycin or Metronidazole

194
Q

Pain in appendicitis

A

Starts out as generalized because of luminal distention carried by general visceral afferents.
Later becomes localized due to somatic irritation of the parietal peritoneum.

195
Q

Pathogenesis of SIADH

A

tumor cell secretes ADH, causing a transient increase in ECF volume; this stimulates enough ANP/BNP to cause salt wasting, which ultimately results in hyponatremia.
Can present as normal volume hyponatremia with HA, weakness, AMS, and seizures

196
Q

What bug is PYR positive?

A

S. pyogenes (GPC)

197
Q

What is the RLS for bile acid synthesis?

A

cholesterol 7a-hydroxylase
converts free cholesterol into acids; the acids are then conjugated to glycine/taurine to form bile salts (more soluble and emulsifiable)

198
Q

Clasp-knife spasticity

A

initial resistance to passive extension, followed by a sudden release of resistance; indicates UMN disease, such as a stroke in M1/IC/CST, or any level on down to the LMN
*IC strokes commonly present as pure motor weakness

199
Q

What bacteria are among the most infectious?

A

Shigella
Campylobacter
Entamoeba histolytica
Giardia lamblia

200
Q

Triad of disseminated gonococcal infection

A
  1. polyarthralgias
  2. skin lesions
  3. tenosynovitis
    * Can also present as purulent arthritis WITHOUT skin lesions
201
Q

What muscle is attached on the medial clavicle?

What muscle is attached on the lateral clavicle?

A

Medial - SCM

Lateral - pect major, deltoid

202
Q

Long-acting BZDs
Short-acting BZDs
Best BZDs in impaired hepatic metabolism

A

Long: diazepam, lorazepam, temazopam, alprazolam, chlordiazepoxide
Short: midazolam, oxazepam, triazolam (MOT)
Best in impaired hepatic metabolism: lorazepam, oxazepam, temazepam (LOT)

203
Q

Symptoms of pancreatic adenocarcinoma of at the head of the pancreas compressing the common bile duct?

A
  • weight loss
  • palpable/enlarged but nontender gallbladder (Courvoisier sign)
  • obstructive jaundice = pruritus, dark urine, pale stools
204
Q

Angiogenesis is driven by what 2 major factors?

A
  1. VEGF - stimulates endothelial cell motility and proliferation
  2. FGF - promotes endothelial cell proliferation, migration, and differentiation; also attracts MPs and fibroblasts for healing
205
Q

What’s the most common presenting symptom of post-procedure atheroembolism?

A

acute kidney injury (oliguria, azotemia); frank infarction with pain/hematuria won’t occur because the emboli are caused by cholesterol, and they are small so you will just find cholesterol clefts in the renal arteries (arcuate or interlobar)

206
Q

What virus causes immortality in cells it infects?

A

EBV - causes B cells to activate and proliferate indefinitely; they continue to produce Ig’s (including heterophiles) and very few release virus particles at a time
*This may increase risk of c-myc translocation and Burkitt lymphoma, or other lymphomas

207
Q

How to differentiate C. botulinum from TCA overdose?

A

C. botulinum - affects both nicotinic and muscarinic; classic 3Ds = diplopia, dysphagia, dysphonia within 12-26hrs of ingestion; +dry mouth
TCA overdose - muscarinic blockade predominates, thus there’d be no effect on NMJ (no diplopia/dysphagia)

How to test the NMJ? - CMAP test, which tests nerve conduction velocities and muscle AP; repetitive stimulation can overcome the botulinum toxin effect and let ACh out (of course this wouldn’t change in TCA OD because there’s no effect on NMJ)

208
Q

Symptoms of organophosphate poisoning

A

Inhibition of AChE, basically ACh overdose:

  1. depolarizing blockade - weakness, paralysis, fasciculations
  2. CNS effects - lethargy, seizures
  3. muscarinic overstimulation - miosis, bradycardia, inc. lacrimation/salivation
209
Q

How to differentiate serotonin syndrome from neuroleptic malignant syndrome? Causes of each?

A
  1. NMS consists of 4: generalized “lead-pipe” rigidity, hyperthermia, ANS instability, and AMS
  2. Serotonin syndrome will usually have hyperactive muscles (instead of rigid, so shivering, clonus, and hyperreflexia) and the hyperthermia/rigidity are way less severe
  3. Causes: neuroleptics, aka antipsychotics, cause NMS; serotonergic medications cause SS
210
Q

What’s the first-line treatment for essential tremor?

A

propanolol

211
Q

What’s the most effective antagonist for chemotherapy-induced vomiting?

A

Serotonergic antagonists (-setrons)
These act via 2 mechanisms:
1. inhibit vagus-mediated stimuli coming in from GI tract
2. block the 5-HT3 Rs in the area postrema/NTS

Remember: area postrema has CTZ; projects to NTS which collects info from AP, GI via CN10, vestibular system, and CNS (i.e., meninges); NTS projects to other nuclei to coordinate vomiting reaction
The other main players in the vomiting center signaling system are M1, D2, H1, and NK1 receptors/substances.

212
Q

Vertical diplopia - described how and indicates what?

A

Described as double vision particularly when looking down and toward the nose, like climbing stairs or reading.
Indicates CN4 palsy, because the SO can’t turn the eye down and in toward the nose.
May see improvement on head tilt away from the side of the lesion.

213
Q

Histologic and clinical appearance of acute viral hepatitis

A

Acute viral hepatitis due to HepA:
Histo: “spotty necrosis” with balloon degeneration, Councilman bodies (eosinophilic apoptotic HCs), and mononuclear cell infiltrates
Clinically: prodrome is fever, malaise, anorexia, N/V, RUQ pain; then within a week later the prodrome goes away and you get signs of cholestasis: jaundice, pruritus, dark urine, and acholic/pale stools; the infection is self-limited and doesn’t progress to chronic hepatitis, cirrhosis, or HCC

214
Q

Vitiligo is caused by

A

a loss of epidermal melanocytes and thereby loss of melanin; etiology is unclear but may be autoimmune

215
Q

Cushing’s vs. Curling’s ulcers

A

These are 2 types of ulcers due to physiologic stress; secondary to impaired mucosal protection against local ischemic injury from HOTN and splanchnic vasoconstriction following shock/severe injury

Cushing = due to intracranial injury, stimulating vagus nerve with acid hypersecretion, causing ulcer in esophagus, stomach, or duodenum that are particularly prone to perforation

Curling = these ulcers arise in the proximal duodenum secondary to severe burns

216
Q

Interstitial myocardial granuloma

A
  • aka Aschoff body
  • pathognomonic for acute rheumatic fever (ARF)-related myocarditis, follows untreated GAS inxn
  • it’s seen on biopsy of the heart and looks like interstitial fibrosis with MPs and LCs plus scattered multinucleated giant cells
  • over time the bodies are replaced by fibrous scar tissue leading to chronic mitral valve regurgitation and stenosis
  • *If you see a myocardial tissue section and there’s a granuloma-like thing in between the myocytes, think Aschoff body
217
Q

Anitschkow cells

A

aka caterpillar cells

  • plump MPs with abundant cytoplasm and slender chromatin ribbons
  • sometimes seen in Aschoff bodies in ARF-myocarditis
218
Q

DDx for cardiac granuloma

A
  • ARF-related Aschoff body
  • sarcoidosis
  • TB, fungal infxn
  • metabolic disorders including Farber’s, gout, and CGD

Non-granulomatous histiocyte infiltration can also occur in Whipple’s disease, Niemann-Pick disease, hyperlipoproteinemias, and Gaucher’s

219
Q

What drugs are used to treat status epilepticus?

A

First line acute: BZDs (diazepam, lorazepam)

First line prophylaxis: phenytoin

220
Q

Drugs used to treat absence seziures

A

First line: ethosuximide

Also: valproate

221
Q

Signs and Ex of small intestine bacterial overgrowth (SIBO)

A
  • high Vitamin K and Folate (DJ Ill has an Iron Fist, Bro)

- Nausea, bloating, abdominal discomfort, malabsorption

222
Q

Relationship between beta-endorphin and ACTH

A

both are produced from POMC precursor

beta-endorphin is an endogenous opioid peptide, and this may be basis of association between stress axis and opioid system

223
Q

How does desmopressin work to treat hemophilia?

A

it increases release of vWF and factor 8 from endothelial cells; really only works on mild hemophilia A, also works on von Willebrand disease

224
Q

Components of the ECM and their functions

A

Hyaluronic acid, Glycosaminoglycans - absorb water and determine stiffness
Fibronectin, Collagen, Laminin - EC structural proteins to which integrins bind

225
Q

Cast nephropathy - think

A

protein

- seen in multiple myeloma from large amounts of bence jones light chain proteins

226
Q

Painless red serpiginous ulcerative lesions - STD?

A

Granuloma inguinale (Donovonosis) caused by Klebsiella granulomatis

  • these are progressive lesions without LAD
  • dx with Gram stain and culture (difficult) or biopsy (donovan bodies)
  • differentiate from syphilis because this won’t have LAD
227
Q

PDGF mutations are in what cancer?

A

Chronic myelomonocytic leukemia

228
Q 
Action; site of release of:
Gastrin 
Somatostatin
CCK
Secretin
GIP
Motilin
A

Gastrin - acid secretion; G cells (antrum, duodenum)
Somatostatin - stop secretions of GI hormones; delta cells (pancreatic islet, gut mucosa)
CCK - release of pancreatic enzymes and bicarb; I cells (SI)
Secretin - panc. bicarb release, stop secreting acid; S cells (SI)
GIP - insulin release, stop secreting acid; K cells (SI)
Motilin - GI motility; M cells (SI)

229
Q

Elderly man with insomnia. What drug class to avoid? Best drug to prescribe?

A

Avoid: BZDs and those with anticholinergic AEs (1st gen Histamine blockers and TCAs)
Good: Ramelteon, melatonin agonist

230
Q

Systemic mastocytosis - common associated mutation and symptoms

A

mutation = KIT (GOF in TK)
Symptoms are derived from the excess histamine released by the mast cells; this causes syncope, flushing, HOTN, pruritus, urticaria, and gastric hypersecretion/ulceration
Other GI sx can include N/V and cramps

231
Q

What does cryptococcus look like under LM?

A

yeast form only with narrow-based buds

*it’s heavily encapsulated (sarcophagus)

232
Q

Adenocarcinoma of the lung

A

Most common
Peripherally located; associated with k-ras, EGFR, and ALK mutations.
In-situ is considered a preinvasive but still malignant mass, it consists of many columnar epithelial cells (w/wo lots of IC mucin) that makes an apparent thickening of the alveolar wall.
Patient may present with copious amounts of expectorate; CXR can have infiltrates that resemble PNA; may also see hypertrophic osteoarthropathy.

233
Q

Causes of aplastic anemia

A

most are direct toxic insult to BM or a T-cell response:
- drugs: chemo, benzene, carbamazepine
- virus: hepatitis, EBV, Parvo B19
In kids the etiology is usually idiopathic.

  • Myelodysplastic syndrome (not really aplastic anemia because there’s many abnormal blasts on BM biopsy) normally occurs in adults >65yo.
  • *Won’t see splenomegaly in AA because there’s no HSCs for extra-medullary hematopoiesis
234
Q

Alcohol withdrawal symptoms and treatment

A
  • Mild sx present within 24hrs: tremulousness, anxiety, insomnia, tremor, diaphoresis, palpitations, GI upset; still orientated
  • Seizures (tonic-clonic) later
    BZDs are first-line to prevent DTs and seizures; long-acting BZDs with active metabolites are good choices: diazepam and chlordiazepoxide
235
Q

Cancers associated with Downs Syndrome

A
  • Myelodysplastic syndrome
  • Leukemia: ALL, and AML (and subtype of AMkL, a variant of which can be transient myelocytic leukemia)
  • Germ cell tumor
236
Q

Non-bacterial thrombotic endocarditis - what is it, and what condition it is associated most with?

A

NBTE aka marantic endocarditis = platelet-rich thrombi attached to mitral valve leaflets
Most commonly associated with advanced malignancy, as well as chronic inflammatory conditions (SLE, antiphospholipid Ab syndrome, and DIC in sepsis)

237
Q

Types of exocrine glands

A
  1. Merocrine - exocytosis; salivary, epocrine, apocrine sweat glands
  2. Apocrine - membrane-bound vesicle secretion; mammary glands
  3. Holocrine - suicide secretion (cell lysis releases everything); sebaceous and meibomian glands (eyelid)
238
Q

What does the Wright-Giemsa stain see when used on blood smear?

A

It will stain blue the remaining nuclear material in reticulocytes - which is actually a reticular network of residual ribosomal RNA

239
Q

Only fungus that can survive intracellularly and cause disease

A

Histoplasmosis

- will see the small ovoid bodies within MPs

240
Q

Appropriate treatment to initiate when someone first shows up with RA

A
  1. Start glucocorticoids/NSAIDs for immediate anti-inflammatory effects
  2. Start DMARD for long-term control; it does take a few weeks to take effect though
    * DMARDs include MTX, Sulfasalazine, Hydroxychloroquine, Minocycline, and TNF-a inhibitors
241
Q

What are the substances that are catabolized into propionic acid?

A

Isoleucine, valine, methionine, threonine, cholesterol, and LCFA
*valine and isoleucine undergo oxidative decarboxylation

Propionyl is then converted to MM-CoA by propionyl CoA carboxylase (uses biotin)

242
Q

What does the suprachiasmatic nucleus do?
Supraoptic?
Arcuate?

A

SCN - senses light, talks to pineal body
Supraoptic - ADH and oxytocin
Arcuate - dopamine, GHRH, and GnRH

243
Q

Where does the gastroduodenal artery run?

Where doe the gastroepiploic arteries run?

A

GD - right behind the duodenum

GE - inferior side of the stomach

244
Q

Does Rifampin act on blocking DNA, RNA, or protein?

A

RNA

  • blocks DNA-dependent RNA polymerase
  • comes with GI side effects, rash, red-orange body fluids and cytopenias
245
Q

DRESS syndrome - what drugs cause it and how does it present?

A

Can be caused by phenytoin, carbamazepine, allopurinol, sulfonamides, minocycline, and vancomycin.
Pts develop fever, LAD, facial swelling, and diffuse morbilliform skin rash, with Eosinophilia and elevated ALT (also atypical lymphocytosis).

246
Q

Symptoms of a VIPoma

A

WDHA syndrome: Watery Diarrhea, Hypokalemia, Achlorhydria
(AKA pancreatic cholera)

VIP binds to epithelial cells–>activates AC–> causes secretory diarrhea; also causes pancreatic bicarb and chloride secretion.

Somatostatin is the inhibitor (just like ‘statins’ inhibit HMG CoA reductase)

247
Q

What happens to Rb in tumor cells?

A

RB gets broken - when active it inhibits G1/S transition; if inactivated by mutation it won’t inhibit the transition

248
Q

Someone has longstanding gallstones; what can happen?

A

cholecystenteric fistula can form between the gallbladder and the small bowel (usually duodenum); the gallstone then gets stuck at the ileocecal valve (usually)
May see air in the gallbladder on imaging (“pneumobilia”) with SBO (abdominal distention, pain, high pitched bowel sounds; and N/V)

249
Q

How to recognize SLE

A

Clinically:

  • fever, fatigue, weight loss,
  • migratory arthralgias, butterfly rash, photosensitivity, serositis
  • thromboembolic events, cognitive dysfunction, seizures

Lab Findings:

  • hemolytic anemia, thrombocytopenia, leukopenia, low C3/C4
  • Anti-smith, Anti-dsDNA
  • proteinuria, elevated creatinine
250
Q

Reaction formation

A

defense mechanism where unacceptable feelings are transformed to the exact opposite

251
Q

NF1 - recognition? genetics?

A
  • patient will have lots of fibromas on the skin, cafe-au-lait spots, optic nerve gliomas, lisch nodules, sphenoid dysplasia, scoliosis, other brain tumors, and pheo’s
  • single mutation, AD, in Chr 17
252
Q

What is the red cell index measure most specific for hereditary spherocytosis?

A

mean corpuscular hemoglobin concentration (MCHC)

253
Q

Why must HepB be there for HepD infection?

A

HepD needs HepB’s surface antigen to get into the hepatocytes

254
Q

Leukemoid reaction - when does it occur, why, and how does it present?

A
  • occurs in the setting of severe infection/sepsis, hemorrhage, malignancy (leukemia), or acute hemolysis
  • it occurs because the bone marrow is spitting out many more mature cells (as opposed to blasts in leukemia) in order to combat the attack
  • presents as LCs >50,000 in the setting of another illness (e.g., pt is febrile with septic PNA)

On blood smear:

  • Dohle bodies - blue/basophilic granules in mature NTs
  • Increased bands (left shift)
  • Toxic granulation
  • Cytoplasmic vacuoles
255
Q

Difference between fractionated and unfractionated heparins?

A

Unfractionated = real heparin, longer; binds AT3 and lets it inactivate Factor Xa; still has extra binding sites for Thrombin so the complex can inactivate it

Fractionated/LMWH = synthetic, shorter, binds AT3 and lets it inactivate Factor Xa; no binding sites for thrombin though (too short)

256
Q

Primary impairment in osteogenesis imperfecta

A

(AD) defective bone matrix formation

  • matrix is formed from collagen and hydroxyapatite crystals
  • the matrix is then mineralized by VitD/Ca process
  • Endochondral ossification = endochondral happens with first a cartilage template, later filled in by deposition of osteoid matrix, then remodeling from woven bone into compact bone
  • intramembranous = no cartilage matrix, straight to osteoid and remodeling
257
Q

Pelvic fracture is most likely to cause injury to the urethra where?

A

At the bulbo-membranous junction (also the post-ant junction) - the weakest portion of the urethra

This is right around the external urethral sphincter, which is like the first 90deg turn, under the prostate

258
Q

Leptin

A

decreases food intake

259
Q

Hibernating myocardium vs. Ischemic pre-conditioning

A

Basically, Hibernating is when there’s prolonged decreased O2 flow to myocardium and it resets. Preconditioning is repeated episodes of angina and that is protective later when there’s a complete occlusion

260
Q

Features of back pain worrisome for metastasis/neoplasm

A
  • pain that is not relieved by rest, position changes, or analgesics
  • worse at night
  • elderly
  • Strong predictor = known history of malignancy
261
Q

Secondhand smoke increases the risk of what in infants?

A
  • SIDS
  • prematurity/low birth weight
  • otitis media
  • asthma
  • URIs, bronchitis, PNA
262
Q

Uremic bleeding

A
  • bleeding due to build-up of toxic products that should be filtered/excreted by the kidney but can’t because of renal failure, such as in a patient on dialysis
  • the toxins prevent platelet aggregation and adhesion, so there’s normal platelet count and coag studies (PT, PTT) but prolonged bleeding time
263
Q

What gives you wrinkles?

A

UVA getting to the cells and producing ROS, which then activate TFs and decrease collagen fibril production - hence less structural support, hence aging
- also activates MMPs which secondarily degrade Type I/II collagen and elastin

264
Q

Obesity gives you what kind of lung disease?

A

Obesity-Related Restrictive Lung Disease

  • this means you have decreased TLC, decreased lung and chest wall compliance due to microatelectasis and increased fat, resp.
  • hallmark is huge reduction in ERV, but no change in RV
265
Q

Traumatic aortic rupture

A

usually from MVCs, it’s a large deceleration that push/pulls the aorta; the ligamentum arteriosum will hold the arch still and allow greater shear forces, which may rupture the aorta at this segment

266
Q

BZDs and Barbiturates on GABA receptor

A

BZDs increase frequency of opening

Barbiturates increase duration of opening (barbiDURATes)

267
Q

Kussmaul sign

A

A rise in JVP on inspiration.
Similar to pulsus paradoxus, it’s a sign of constrictive pericardial disease because normally on inspiration the venous return increases, but if constricted the R heart can’t open to accommodate the increased volume, and thus it backs up into the jugular.

268
Q

How to recognize Lipofuscin

A

the wear and tear pigment - it’s yellow-brown intracytoplasmic, perinuclear granules; the product of free-radical and lipid peroxidation

** “Lipo” = lipid

269
Q

Industrial exposure to rubber, aromatic amine dyes, textiles, leather increases risk of what cancer?

A

transitional cell carcinoma of the bladder

270
Q

How does spironolactone cause gynecomastia?

A

It’s an aldosterone antagonist
But it also acts as an androgen receptor antagonist (structurally similar to androgens), and thereby inhibits testosterone synthesis; without the testosterone to be converted to DHT, breast tissue will grow

*Eplerenone is a newer spironolactone type drug that has fewer side effects

271
Q

What do neurons look like after an axon is severed?

A
  1. proximal portion of the neuron = Neuronal Reaction; the cell body swell, nucleus and Nissl moves to the side (central chromatolysis), seen 24-48hrs after injury and peaks around 12d
  2. distal/severed axon = Wallerian degeneration; swelling and irregularity of the axon, then w/in 7d the Schwann cells and MP digest the fragments
272
Q

Hemosiderin

A

coarse yellow-brown pigment that comprises iron complexes from the blood; can be in Kupffer cells like in chronic hemolysis, or in MPs in the lungs like in heart failure

273
Q

Pathophys difference between gastric and duodenal ulcers

A

Both are the result of damage to the segment’s defense against acid:
Gastric = damaged mucus layer (and associated inflammation) allows acid to hurt to gastric cells; acid amount will be low to normal
Duodenal = used to having lots of acid dumped, so ulcers here will appear if there’s decreased somatostatin (D cells) or pancreatic bicarb released

*H. pylori and NSAIDs are MCC of duodenal ulcers, but keep in mind ZE syndrome from gastrinoma

274
Q

Kidney disease and c-ANCA+ - think:

A

Wegener’s, and rapidly progressive GN (so crescents)
*May also see: necrotizing granulomas in the lungs (so cough/hemoptysis) and ulcerating granulomas in the URT (chronic sinusitis, ENT)

275
Q

Ristocetin

A

activates Gp-Ib receptors on platelets for them to bind vWF

276
Q

Heroin/Opioid withdrawal

A 
Specific = lacrimation and yawning
Others = dilated pupils, piloerection, hyperactive bowels, N/V, abdominal cramps
277
Q

Alcohol vs. BZD withdrawal

A

Both will have tremors, anxiety, psychosis, tachycardia, palpitations, and seizures.
Alcohol will also have delirium.
BZDs will also have perceptual disturbances and insomnia.

278
Q

How long does ischemic myocardial tissue last?

A

30min - after that the damage is irreversible

279
Q

What cancers are most commonly associated with paraneoplastic syndrome causing Dermatomyositis?

A

ovarian, lung, and colorectal adenocarcinoma, and non-Hodgkin lymphoma
**Remember Dermatomyositis = proximal muscle weakness with heliotrope rash and rash on knuckles (whereas SLE will affect skin in between knuckles)

280
Q

What is stimulus control in sleep therapy?

A

it’s re-associating the bedroom with sleep only and nothing else

281
Q

How does Vitamin K help babies?

A

Vit K is a cofactor needed for gamma-glutamyl carboxylase, which is the enzyme that synthesizes Factors 2,7,9,10
- without it working babies will bleed, i.e. ICH, GI, cutaneous, umbilical, and surgical bleeding

282
Q

Which enzymes give what information about the following:
liver
biliary tree

A

Liver functionality - PT, albumin, bilirubin, cholesterol
Livers structural integrity/cellular intactness - ALT, AST
Biliary tree structural integrity/cellular intactness - Alk-phos, gamma-glutamyl transferase

*When there’s an elevated Alk-phos, you can’t tell if it’s from biliary tract or bone; check GGT because if elevated then you know the problem is in the biliary tree/biliary epithelium

283
Q

VPN is a growth medium containing what? used for what?

A 
Used for Neisseria species
- Vancomycin - inh. GP bacteria
- Polymixin, aka Colistin - inh. other GN bact
- Nystatin - inh. yeast
\+/- Trimethoprim - inh. Proteus species

Chocolate agar can also grow Neisseria, but not regular blood agar

284
Q

Cancer from Ulcerative Colitis - development, mutations, risk factors

A

Develops from flat, dysplastic lesions (not polypoid, as in other types or sporadic CRC).
Mutations include p53 early on, leading to a less differentiated form at presentation (classic sporadic pathway goes APC –> k-ras –> p53).
Pancolitis has the highest risk of CRC, and extent and duration of colitis are the strongest risk factors for development of CRC.

285
Q

Food-related areas of Hypothalamus

A

Ventromedial - mediates satiety; destroy and won’t be satisfied, will get fat
Lateral - mediates hunger; destroy and won’t be hungry, will get skinny

286
Q

Anterior and Posterior Hypothalamus

A

Anterior - regulates heat dissipation; destroy and all heat will be kept, get hyperthermia
Posterior - mediates heat conservation; destroy and all heat wil be lost, get hypothermia

287
Q

Most important risk factor for intimal tears leading to aortic dissection

A

HTN

288
Q

Watershed areas of the large bowel

A

splenic flexure and rectosigmoid junction

289
Q

How long does it take to reach steady-state?

A

ABout 4-5 half lives for a first-order kinetics drug
That’s because in 1 HL –> 50% of steady state
2 HL –> 75%
3 HL –> 87.5%
etc.

290
Q

What is the Periodic Acid stain good for?

A

highlighting glycoproteins, such as those found in fungal cell walls, mucosubstances secreted by epithelia, and basement membranes

291
Q

Cystic medial degeneration

A

the process of myxomatous change in the media of blood vessels that weakness the CT and can lead to aneurysm formation; a major cause of which is Marfan syndrome

292
Q

Causes/Associations of:
SCC of esophagus
Adenocarcinoma of esophagus

A

SCC - associated with alcohol and smoking in US; associated with chewing betel nuts and foods with N-nitroso compound in Asia

Adenocarcinoma - associated with GERD and Barett’s (fatty diets and obesity) in the US; hot beverages in Asia

293
Q

What are the 3 types of PNA, and of the lobar type what are the 4 stages?

A

3 types = bronchopneumonia, interstitial, lobar
Lobar 4 stages =
1. congestion (24hr) - alveolar exudate just bacteria
2. red hepatization (2-3d) - red and firm with RBCs, NTs, and fibrin in exudate
3. gray hepatization (4-6d) - RBCs go away (“disintegrate”, “fragmented”)
4. resolution - restoration of normal, exudate is digested

294
Q

What’s the main pathophysiology in PCV?

A

the activating mutation in the JAK2 gene renders HSCs more responsive to growth factors like EPO/TPO

295
Q

People with SCD or SCT - what infections will they get? What kind of kidney damage?

A

They will get infected with encapsulated organisms (SHiNE SKIs - MC is Strep pneumo, #2 is H. flu).
They will get renal papillary necrosis which presents as gross hematuria (passage of blood clots) without pain.

296
Q

What two substances will be elevated in NTD?

A

AFP

AChE

297
Q

How does Acetyl-CoA help with gluconeogenesis?

A

it serves as an allosteric activator of the first step – which is pyruvate carboxylase (converts pyruvate to oxaloacetate for going back to PEP)

298
Q

Beta-blocker OD:

What’s happening and How to treat

A

Happening: blocked beta-receptors means myocardial contractility depression, bradycardia, and heart block
Treatment: glucagon, will act on GPCRs, increase IC cAMP and restore cardiac contractlity

299
Q

Where are dietary fats absorbed?

A

in the jejunum!!
not the duodenum - in duodenum they are just chopped up by pancreatic lipases and emulsified by bile salts; it’s not until the jejunum that they’ve mixed enough and get into close contact with the wall for passive absorption

300
Q

Immature myeloid cells + low fibrinogen makes you think

A

APL (M3 subtype of AML) with t(15;17) translocation
*may also have description of immature myeloid precursors in BM biopsy
The low fibrinogen is a consumptive bleeding because the patient will be in DIC
Don’t forget the Auer rods

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