UWorld Practice Questions #3 Flashcards

1
Q

Lesions to the macula (i.e. drusen deposition in condition of macular degeneration) will produce what?

A

Central scotomata which is visual field defect to the center of vision, surrounded by areas of normal vision. This is b/c the macula does the center of our vision and has the highest level of acuity.

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2
Q

How does Kawasaki disease present and what is a serious complication of it?

A

Presents w/ fever of 5+ days plus: bilateral non-exudative conjunctivitis, cervical lymphadenopathy, mucositis (fissured lips, strawberry tongue), edema of hands and feet, erythema of palms and soles, and rash.

A serious complication is coronary artery aneurysm.

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3
Q

What type of media is Thayer-Martin media?

A

Selective media –> antibiotics kill potential contiminants

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4
Q

What characterized erectile disorder?

A

Persistent inability to attain or sustain an erection.

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5
Q

The deep inguinal ring is a physiologic opening in the _____, and the superficial inguinal ring is a physiologic opening in the _______?

A

Deep inguinal ring –> transversalis fascia

Superficial inguinal ring –> external oblique muscle apopneurosis.

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6
Q

What sort of drugs are aprepitant and fosaprepitant? What are they used for?

A

They are neurokinin-1 (NK1) receptor antagonists. NK1 is one of the receptors involved in the vomiting reflex so these meds can be used for acute and delayed vomiting induced by chemotherapy, that is refractory to more traditional chem anti-emetic tx like ondansetron and metoclopramide.

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7
Q

What is allocation bias?

A

Bias in a study that results from non-random allocation into the different study groups. For example, physicians may enroll sicker patients into the experimental arm of a study - this would be allocation bias.

Note that this is DIFFERENT from selection bias where the issues is the study population does not represent the intended population.

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8
Q

What is detection bias?

A

Where a risk factor for something results in more extensive workup and thus a greater likelihood of finding something. Example –> smoking pts undergoing more imaging so cancer is detected more often.

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9
Q

What is the presentation of norepinephrine extravasation and how do you treat it?

A

Blanching of a vein into which norepi is being infused plus induration, pallor, hardness and coolness to the surrounding area is a sign of this condition (where norepi is leaking causing vasoconstriction and potentially tissue necrosis)

Tx = local injection of an alpha blocker like phentolamine.

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10
Q

How does the drug clomiphene work?

A

It is a selective estrogen receptor modulator that prevents the negative feedback of estrogen on the hypothalamus and pituitary by circulating estrogen. This results in increased LH and FSH production and ovulation.

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11
Q

In Friedrich-Ataxia, where does neural degeneration occur?

A

In the spinocerebellar tracts, lateral corticospinal tracts, dorsal columns and dorsal root ganglia.

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12
Q

How does gestational choriocarcinoma present? How does it appear histologically?

A

Presents w/ vaginal bleeding, uterine enlargement and an abnormally elevated BHcg. Also, can get hemoptysis as it is a rapidly aggressive tumor whose most common met site is the lung.

Histo shows abnormal proliferations of cytotrophoblasts and sycytiotrophoblasts. No villi are present.

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13
Q

In an orbital floor injury (i.e. from getting socked in the face while getting molly-whapped in a bar fight) allows the contents of the orbit to herniate into what area?

A

The maxillary sinus.

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14
Q

What is the most important prognostic factor for post-streptococcal glomerulonephritis?

A

Increased age. Only 60% of adults fully recover while the rest develop stuff like persistent HTN, rapidly progressive GN, recurrent proteinuria and chronic renal insufficiency.

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15
Q

Describe the most common pathogenesis to infective endocarditis?

A

First is disruption of the normal endocardial surface, which occurs most commonly via turbulent blood flow leading to focal adherence of fibrin and platelets. This forms a sterile fibrin-platelet nidus to which bacteria can then bind and colonize.

Note that S. aureus is unique in that it can adhere to normal or damaged endothelial cells.

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16
Q

What does the Nissl substance in neurons represent?

A

The rough endoplasmic reticulum.

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17
Q

Histologically, what characterizes acute neuronal injury (ultimately leading to cell death)?

A

Shrinkage of the cell body, pyknosis (irreversible condensation of chromatin) of the nucleus, loss of nissl substance and an eosinophilic cytoplasm.

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18
Q

Histologically, what characterizes an axonal reaction (where a neuron’s axon is severed)?

A

Cell body enlargement, nucleus moves to the periphery, enlargement of the nucleuolus, and dispersion of the Nissl substance.

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19
Q

What makes up the calcifications seen on imaging in craniopharyngiomas?

A

Cholesterol crystals. Why on macroscopic exam they can be cystic w/ a high cholesterol content.

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20
Q

Micrognanthia, prominent occipt, clenched hands w/ overlapping fingers and low set ears in a newborn is most likely indicative of what trisomy?

A

Trisomy 18 (Edward syndrome)

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21
Q

What neonatal condition does a 5p deletion cause?

A

Cri-du-chat syndrome. Pts have cat-like cry as well as hypotonia, failure to thrive and developmental delay.

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22
Q

What are degmacytes?

A

Bite cells

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23
Q

Compared to hexokinase, glucokinase (which is present in hepatocytes and B cells) has a ____ Km and ______ Vmax

A

Higher Km (meaning less affinity for glucose) and higher Vmax

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24
Q

What are the essential amino acids? List them including whether they are glucogenic, ketogenic or both.

A

Glucogenic: methionine, valine, and histidine (his is only essential during periods of growth as body can’t make enough then)

Ketogenic: isoleucine, phenylalanine, threonine and tryptophan

Glucogenic/ketogenic: leucine and lysine

*Note that arginine is like histidine in that it is essential during periods of growth.

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25
Q

What is the treatment for methemoglobinemia?

A

Methylene blue. It is has been shown to help w/ the conversion of iron back into ferrous (2+) form.

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26
Q

What are some drugs that can cause methemoglobinemia?

A

Oxidizing agents like dapsone, sulfonamides, and local anesthetics like benzocaine

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27
Q

What is thiosulfate used to treat?

A

Cyanide poisoning.

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28
Q

What is the thyroid’s embryological origin?

A

Thyroid diverticulum arises from the floor of the primitive pharynx.

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29
Q

What are perioxisomes involved in the metabolism of?

A

Very long chain fatty acids, branched chain fatty acids, amino acids, and ethanol.

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30
Q

What is the most common form in which mutations that produce Duchenne muscular dystrophy occur?

A

Frameshift mutation

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31
Q

What do Ca, P and alk phos labs show in osteoporosis? How about Paget’s disease?

A

Osteoporosis –> normal Ca, normal P, and normal or decreased alk phos

Paget’s disease –> normal Ca and normal P w/ elevated alk phos.

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32
Q

Why can acute ethanol intoxication lead to lactic acidosis and hypoglycemia?

A

Booze leads to increased NADH:NAD+ ratio (b/c of the oxidation of metabolizing alcohol). This ratio shunts pyruvate to lactate formation and this both creates the acidosis (lactic acidosis) and causes hypoglycemia as there is not enough pyruvate available to do gluconeogenesis.

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33
Q

Which atypical antipsychotic is most strongly associated w/ galactorrhea as a side effect?

A

Risperidone

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34
Q

Which malignancies are most likely to metastasize to the bone?

A

Prostate/Breast > Kidney/Thyroid/Testes/Lung

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35
Q

What are “slow waves” in the GI tract?

A

They are rhythmic depolarizations and repolarizations of the smooth muscles cells within the muscularis propria of the stomach and intestines. Slow waves determine the frequency of contractions of the gastrointestinal tract.

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36
Q

What is an adverse effect from fluoroquinolones to know about and who is at increased risk?

A

Tendinitis. Increased risk = old, renal disease (transplant, hemodialysis, etc), and long term glucocorticoid use.

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37
Q

What is the first line treatment for diabetic gastroparesis?

A

Metoclopromide

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38
Q

What is rheumatoid factor?

A

It is antibody (typically IgM) against the Fc component of IgG.

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39
Q

What do anti-phospholipid antibodies (found in SLE and antiphospholipid antibody syndrome) cause?

A

A hypercoagulable state w/ paradoxically increased PTT.

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40
Q

What are the characteristics of CREST syndrome?

A

Calcinosis, Raynaud’s phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia.

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41
Q

What is the most common mutation causing idiopathic pulmonary arterial hypertension (PAH) and what does this cause?

A

BMPR2 gene which predisposes pts to dysfunctional endothelium and smooth muscle proliferation. A second insult leads to vascular remodeling, increased resistance, and ultimately leads to PAH.

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42
Q

What are the most common pathogens that pts w/ CGD are susceptible to?

A

Catalase + ones, most common being S. aureus, Burkholderia cepacia, Serratia marcescens, Norcardia and Aspergillus.

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43
Q

Which virus is associated w/ fulminant hepatitis in pregnant women? How would you characterize it?

A

Hepatitis E virus. It is a naked ssRNA viral spread via fecal oral route.

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44
Q

What shape are cysteine renal stones?

A

Hexagonal. They are radio opaque.

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45
Q

What is the microscopic shape of magnesium ammonium phosphate stones (aka struvite stones)?

A

They are prism shaped and can be described as coffin lid shaped. They are radio opaque.

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46
Q

What kind of drug is canagliflozin?

A

SGLT2 inhibitor.

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47
Q

What is the pathogenesis, presentation and dx of Hartnup disease?

A

It is a genetic defect in the neutral amino acid transporter such that pts get impaired transport of neutral amino acids in the intestine and proximal renal tubule. Tryptophan is a neutral amino acid and a precursor for niacin and so this disorder causes niacin deficiency and basically has a pellagra-like presentation (including cerebellar ataxia in childhood).

Dx is by presence of excessive amounts of neutral amino acids in the urine.

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48
Q

What is the most common cause of thoracic outlet syndrome?

A

Compression of the lower trunk of the brachial plexus in the scalene triangle, btwn the anterior and middle scalene muscles

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49
Q

What is diphenoxylate?

A

An opioid anti-diarrheal.

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50
Q

Meconium ileus is a very specific finding for what disease?

A

CF

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51
Q

What enzyme is deficient in patients with xeroderma pigmentosum?

A

UV specific endonuclease. As such they cannot repair the thymidine dimers caused by UV exposure and get photosensitivity, hyperpigmentation and can even get skin cancers.

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52
Q

What histologic changes characterize minimal change disease?

A

Normal light and immunofluorescence microscopy. Effacement of foot processes can be seen on electron microscopy.

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53
Q

What causes the selective albuminuria in minimal change disease?

A

Loss of the negative charge at the glomerular basement membrane that allows positively charged albumin to escape.

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54
Q

Crescent formation is most typically associated w/ which glomerular disease?

A

Rapidly progressive glomerulonephritis

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55
Q

What histologic changes characterize diabetic nephropathy?

A

Mesangial expansion and glomerular basement membrane thickening. Kimmelstiel-Wilson lesions are specific for this and they are ovoid or spherical hyaline (eosinophilic) masses found in the mesangium.

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56
Q

What brain lobe does the Meyer’s loop travel in? As such, what visual defect does damage produce?

A

Travels in the temporal lobe so damage produces the “pie in the sky” defect.

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57
Q

What sort of receptor is the glucagon receptor?

A

Gs GPCR

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58
Q

Why is PaO2 normal in carbon monoxide poisoning?

A

Because PaO2 is a reflection of the amount of O2 dissolved in the blood and this is unchanged by CO. Instead, CO is changing the oxygen carrying capacity of Hgb in the blood, and is L shifting the Hgb-O2 dissociation curve.

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59
Q

What is the main measure of association reported in case-control studies? How is it calculated?

A

Odds ratio. Incidence measures like relative risk cannot be calculated b/c by definition patients already have the disease.

OR = odds of exposure in cases / odds of exposure in controls

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60
Q

Describe the pathogenesis of a lacunar infarct?

A

These occur in the small penetrating arterioles of deep brain structures. Chronic HTN promotes lipohyalinosis, microatheroma and hardening/thickening of vessels walls leading to formation which narrows vessels and predisposes to thrombotic infarct. After several weeks the necrotic spaces turn into fluid filled cavities called lacunae.

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61
Q

Intra-operative rupture of hydatid cysts (caused by echinococcus) can be lethal how?

A

Spilling of cyst contents can lead to anaphylactic shock.

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62
Q

What makes up the 3’ end of tRNA?

A

CCA

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63
Q

In duodenal ulcers secondary to H. pylori, where is the GI tract does the bug preferentially colonize?

A

The gastric antrum. Note that in gastric ulcers, it is associated w/ colonization of the gastric body.

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64
Q

In ischemic acute tubular necrosis (ATN), what parts of the nephron are most vulnerable to ischemic injury?

A

The proximal tubule and thick ascending limb of the loop of Henle.

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65
Q

What is CEA elevated in and what can it be used for?

A

Carcinoembryonic antigen (CEA) is elevated in breast, gastric and pancreatic malignancies (as well as some benign diseases like IBD). It can be used as a sensitive marker for cancer residual disease after surgery and colorectal cancer recurrence.

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66
Q

What are 2 classic manifestations of pineal gland tumor? Why?

A

1 = obstructive hydrocephalus (headache, papilledema, vomiting) due to aqueductal stenosis

2 = Parinaud syndrome due to compression of the pretectal region of the midbrain. This presents w/ limitation of upward gaze, bilateral lid retraction, and pupils that react to accommodation but not light.

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67
Q

Why can ACEIs and ARBs cause oligohydramnios when used during pregnancy?

A

Because angII is necessary for renal development.

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68
Q

It is very important to screen all patients with major depressive for what?

A

A past hx of mania so that the distinction can be made between MDD and bipolar disorder. This is really important in order to ensure that pts get the correct tx.

Antidepressant monotherapy should be avoided in patients with bipolar as this can precipitate mania (tx emergent mania).

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69
Q

Wilson disease is associated w/ cystic degeneration of what brain area?

A

The putamen

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70
Q

Calmodulin is important for excitation-contraction coupling in which cells?

A

Smooth muscle cells as they lack troponin.

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71
Q

What do neurophysins do?

A

They act as carrier proteins for oxytocin and ADH from the paraventricular and supraoptic hypothalamic nuclei respectively, to the posterior pituitary.

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72
Q

In inferior colliculi and medial geniculate bodies are part of?

A

The auditory pathway

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73
Q

In idiopathic intracranial HTN (most commonly seen in young, obese women), when do sxs characteristically worsen?

A

During valsalva so doing stuff like bending over, lifting objects, coughing, etc.

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74
Q

Describe the pathophysiology of optic disc edema in increased intracranial pressure:

A

Increased ICP is transmitted thru CSF to subarachnoid space which is continuous w/ the optic nerve sheath. This pressure build-up compresses the optic nerves externally and this impairs axoplasmic flow which results in the papilledema.

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75
Q

Choroidal inflammation of the eye is characteristic of?

A

Posterior uveitis.

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76
Q

What is the most significant risk factor for UTI while a pt has a catheter?

A

Duration of catheterization

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77
Q

Where does Parvovirus replicate?

A

In erythrocyte precursors in the bone marrow

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78
Q

What is the mechanism of action of adenosine?

A

It causes hyperpolarization of AV nodal cells, briefly blocking conduction thru the AV node.

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79
Q

What is the most common location for osteonecrosis (avascular necrosis) and what are common predisposing conditions?

A

Femoral head = most common location. Predisposing conditions include sickle cell disease, glucocorticoid use, alcoholism and vasculitis.

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80
Q

What is the use and mechanism of action of azathioprine? What is its interaction w/ allopurinol?

A

It is the prodrug of 6-mercaptopurine and the active form works by inhibiting de novo purine synthesis –> suppresses the immune system by blocking lymphocyte proliferation due to blocked nucleotide synthesis.

Xanthine oxidase is one of the metabolism pathways by which azathioprine is degraded so by blocking XO w/ allopurinol there is more drug that is converted into the active for.

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81
Q

How does tacrolimus work and what is it used for?

A

It is an immune suppressant. Works by inhibiting calcineurin and blocking T cell activation by preventing IL-2 transcription.

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82
Q

What is the mechanism of action of rifamixin in treating hepatic encephalopathy?

A

It is a non-absorbable antibiotic that alters GI flora to decrease the intestinal production and absorption of ammonia.

*note that a primary source of ammonia is intestinal breakdown of nitrogenous products by bacteria.

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83
Q

What does the ristocetin aggregation test measure?

A

In vitro vWF dependent platelet aggregation.

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84
Q

Bernard-Soulier syndrome is hereditary deficiency of what?

A

GP Ib receptors

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85
Q

Glanzmann thrombocytopenia is hereditary deficiency of what?

A

GP IIb-IIIa receptors

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86
Q

How does C. diphtheriae acquire its virulence that causes pseudomembranous pharyngitis?

A

Through bacteriophage-mediated infection with the Tox gene, which codes for the diphtheria AB exotoxin.

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87
Q

What is spongiosis? Name a dermatological condition that demonstrates it?

A

Spongiousis is an accumulation of edema fluid in the intercellular spaces of the epidermis. It is seen in acute allergic contact dermatitis.

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88
Q

CD15+ and CD30+ is characteristic staining for…

A

Reed-Sternberg cells in Hodgkin’s lymphoma.

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89
Q

Isolated cleft palate occurs due to failure of…?

A

Fusion of the lateral palatine processes, the median palatine processes, and/or the nasal septum

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90
Q

What does alpha-amantin (a toxin found in mushroom caps) inhibit?

A

RNA polymerase II

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91
Q

What cells produce intrinsic factor?

A

Gastric parietal cells

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92
Q

What is the pathogenesis of I-cell disease? How does it present?

A

Pathogenesis = failure to add mannose-6-P residues to proteins that should be directed to the lysosome.

Presentation = course facial features, developmental delay, clouded corneas, restricted joint movement and elevated lysosomal enzymes.

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93
Q

What is a Michaelis-Menten constant?

A

Same thing as Km. It is the concentration of substrate at which a reaction operates at 1/2 Vmax. Thus, it is a reflection of an enzyme’s affinity for substrate.

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94
Q

Is it bullous pemphigoid or pemphigus vulgaris that has a + Nikolsky sign?

A

Pemphigus vulgaris. This means the blisters/bullae rupture easily.

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95
Q

______ has the finding of morula w/in the cytoplasm of granulocytes while _______ has the finding of morula w/in the cytoplasm of monocytes?

A

Granulocytes –> anaplasmosis

Monocytes –> erlichiosis

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96
Q

Which type of electromagnetic radiation is thought to be the major contributor to melanoma?

A

UVB rays.

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97
Q

What is the equation for total peripheral resistance for a parallel circuit?

A

1/Rt = 1/R1 + 1/R2 + 1/R3 etc.

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98
Q

What is unique about the L type Ca++ channels in skeletal muscle as compared to smooth muscle or cardiac muscle?

A

They interact directly with the ryanodine receptor –> mechanical coupling.

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99
Q

What kind of drug is chlorpheniramine?

A

It is a first generation anti-histamine

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100
Q

How is a dx of tetanus made?

A

Clinically, by hx and PE.

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101
Q

What type of drug is octreotide?

A

Somatostatin analog.

102
Q

What is the single greatest RF for aortic dissection?

A

HTN is the greatest RF for intimal tears which is the inciting event in the pathogenesis of aortic dissection.

103
Q

What is one potential adverse consequence of oxygen therapy that is administered to treat neonatal respiratory distress syndrome? Describe the pathogenesis of how it is believed this occurs.

A

Retinal damage. Temporary hyperoxia of the retina is thought to induce changes that up-regulate the expression of pro-angiogenic factors (like VEGF) on return to room air ventilation. This leads to retinal neovascularization and possible detachment with the consequence of blindness. This condition is called retinopathy of prematurity or retrolental fibroplasia.

104
Q

What is terbutaline used for?

A

It is a tocolytic drug used to delay labor by suppressing uterine contractions.

(makes sense b/c it is a B2 agonist - acting at the uterus to promote relaxation)

105
Q

What causes an S3 gallop to develop?

A

Left ventricle volume overload –> forceful rapid passive filling of the ventricle that exceeds the expansion capacity of said ventricle leads to sudden deceleration of blood entering and reverberation of the ventricular walls.

This sound develops in the setting of dilated cardiomyopathy (systolic HF), as well as aortic or mitral regurg.

106
Q

What causes an S4 to develop?

A

It is the sound of blood being forced into a stiff ventricle. As such, it reflects diastolic dysfunction/diastolic HF (i.e. left ventricular hypertrophy).

107
Q

What is the pathogenesis of superior mesenteric artery syndrome? What commonly causes it?

A

It is when the transverse portion of the duodenum becomes entrapped btwn the aorta and the SMA due to critical decrease in the aortomesenteric angle. Associated w/ stuff like diminished mesenteric fat, pronounced lordosis or surgical correction of lordosis.

108
Q

Which anti-arhythmic known to prolong to QT interval has the lowest risk of causing torsades for these drugs?

A

Amiodarone.

109
Q

E. coli is indole ________ while enterobacter cloacae is indole _______

A

E coli –> positive

Enterobacter –> negative

110
Q

What is the capsule of H. flu made of

A

A polymer of polyribosylribitol phosphate (PRP)

111
Q

Where is the damage in ALS?

A

Anterior horns and cortical spinal tracts

112
Q

What effects on the heart would be characteristic of carcinoid syndrome?

A

Endocardial thickening and fibrosis of the tricuspid and pulmonic valves. This can lead to R sided HF.

113
Q

Name 3 causes of hyperosmotic volume contraction?

A

Diabetes insipidus, profuse sweating (sweat is hypotonic), and decreased fluid intake (aka dehydration).

114
Q

Prostate cancer bone mets are commonly … ?

A

Osteoblastic (meaning sclerotic)

115
Q

Murmur of mitral regurg?

A

Holosystolic murmur best heart at the apex, that radiates to the axilla.

116
Q

What sort of erythrocytes are seen in lead poisoning?

A

Erythrocytes w/ basophilic stippling

117
Q

What causes ringed sideroblasts to form and where are they seen?

A

They form in response to inhibitions of the heme synthesis pathway (as they are precipitations of iron granules in developing erythrocytes) and are seen in the bone marrow.

118
Q

How does long term exposure to estrogen (i.e. pregnancy or hormone replacement in post-menopausal women) affect thyroid hormone levels?

A

Estrogen will stimulate production of thyroxine binding globulin (TBG). This results in a transient increase in thyroid hormone production until TBG is saturated again. The net result is increased total pool of T4 with stable levels of free T4.

119
Q

What is the mechanism of action of buspirone?

A

It is a non-benzo anxiolytic that has partial agonist activity at the 5HT1A receptor. It has a slow onset of action (clinically takes at least 2 weeks usually) and can be used to treat generalized anxiety disorder.

120
Q

What are some differences btwn buspirone and benzos

A

Buspirone lacks anti-convulsant and muscle relaxant activity, it does not cause euphoria and has no risk of tolerance, dependence or withdrawal.

121
Q

How does a chronic arteriovenous fistula affect cardiac parameters?

A

Increased CO, increased venous return and decreased total peripheral resistance.

122
Q

Why do pts with long standing COPD having more of a hypoxic respiratory drive? Where are the sensors for said drive?

A

Normally, central chemoreceptors in the medulla drive respiration based on PaCO2 levels. However, pts w/ longstanding COPD have chronic hypercapnia so these centers get less sensitive. Additionally, they have chronic hypoxemia so that while normally O2 contributes little to respiratory drive (healthy people), it becomes a major contributor for these pts.

Peripheral chemoreceptors sensing O2 are located in the carotid and aortic bodies.

123
Q

What is there deposition of in pseudogout?

A

Pyrophosphate

124
Q

Why can myeloproliferative disorders like polycythemia vera predispose a patient to gout?

A

Because myeloproliferative disorders lead to increased production of urate.

125
Q

What are two stimuli for renin release?

A

sympathetic stimulation of B1 receptors, and decreased renal blood flow.

126
Q

Which pattern of lung disease has a decreased FEV1/FVC ratio?

A

Obstructive lung disease.

127
Q

Where does isoproterenol have action?

A

Agonist at B1 and B2 receptors

128
Q

What is the principle site of norepinephrine synthesis in the brain? Where is it located?

A

The locus ceruleus. It is located in the posterior rostral pons, near the lateral floor of the 4th ventricle.

129
Q

When does L ventricular myocardial perfusion occur?

A

Mainly during diastole

130
Q

What is the only DNA polymerase w/ 5’ to 3’ activity (useful for stuff like removing RNA primers)?

A

DNA polymerase I. All prokaryotic DNA polymerases have 3’ to 5’ proofreading exonuclease activity.

131
Q

What is the mechanism of action of triptans?

A

They are 5HT1B/1D receptor agonists. This inhibits the release of vasoactive peptides, promotes vascoconstriction and blocks pain pathways in the brainstem - which is what yields their efficacy for abortive therapy for migraines.

132
Q

Describe the pathophysiology w/ which uremia can lead to excessive bleeding

A

Uremic toxins accumulate (i.e. ESRD) and they inhibit platelet aggregation and adhesion. This leads to a qualitative platelet disorder where there is prolonged bleeding in the setting of normal PT, aPTT and platelet count.

133
Q

What sort of adrenergic receptors does the uterus have?

A

B2 (stimulation leads to uterine relaxation)

134
Q

What is the most common cause of death in Friedrich Ataxia?

A

Complications from hypertrophic cardiomyopathy.

135
Q

Of the adenomatous colon polyps, which type is more likely to undergo malignant transformation?

A

The villous type is more likely to undergo malignant transformation than the tubular type.

136
Q

In what condition are anti-topoisomerase I (aka anti-Scl-70) antibodies seen?

A

Systemic sclerosis –> diffuse scleroderma type

137
Q

What are anti-centromere antibodies specific for?

A

CREST syndrome (the other variant of scleroderma)

138
Q

What are anti-Ro/SSA and anti-La/SSB found in?

A

Sjogren syndrome

139
Q

When is FGF-23 released and what does it do?

A

Released by osteocytes and osteoclasts in response to high phosphate levels (i.e. renal osteodystrophy) and it works to decrease proximal tubule phosphate reabsorption.

140
Q

What does lung silicosis appear like on histology? What distinguishes it on CXR?

A

Histo –> Birefringent particles surrounded by fibrous tissue.

CXR –> calcification of the rim of hilar nodes (eggshell calcification)

141
Q

What is seen on histo in asbestosis? What can be seen on CXR?

A

Histo –> ferruginous bodies which are fusiform rods w/ a translucent asbestos center and an iron containing coating.

CXR may show pleural plaques

142
Q

What is seen on histo in beryliosis?

A

Non-caseating epitheloid granulomas w/o obvious, associated particles.

143
Q

Why can A1c be falsely low in diabetics w/ beta thalassemia trait?

A

B/c A1c reflects extent of hyperglycemia that erythrocytes are exposed to, but also duration of exposure. The microcytic cells in B thal trait are more prone to hemolysis and thus have shorter lifespan. This means less duration of hyperglycemia exposure and thus an artificially low A1c.

144
Q

What causes the voluminous post-prandial diarrhea and weight loss in short bowel syndrome?

A

Excessive malabsorption of macro and micronutrients (due to loss of absorptive surface area).

145
Q

Huntington’s is characterized by deficiency of what neurotransmitter?

A

GABA. This is due to loss of GABA containing neurons in the striatum.

146
Q

What are the main sxs of fibromyalgia?

A

Widespread musculoskeletal pain, fatigue, and impaired attention/concentration. PE shows multi points of tenderness but absence of joint or muscle inflammation.

147
Q

Describe the presentation of dermatomyositis

A

Bilateral proximal muscle weakness, violaceous eruption of eyelids and knuckles, and elevated creatinine kinase levels.

148
Q

Describe the presentation of polymyalgia rheumatica

A

Inflammatory disorder affecting pts 50+ y/o. Subacute pain in shoulders and hips, weight loss, fever and malaise.

149
Q

What is the mechanism of action of terbinafine?

A

It inhibits ergosterol synthesis by inhibiting squalene epoxidase

150
Q

What is germinal matrix fragility responsible for?

A

Intraventricular hemorrhage in premature infants.

151
Q

Describe the presentation of seborrhic dermatitis

A

Itchy, ill-defined erythema and greasy scaling involving the scalp, nasolabial fold or post-auricular skin.

152
Q

Where is atopic dermatitis usually seen in adults?

A

Flexural surfaces. (I believe it can be seen on the cheeks when it occurs in really little kids).

153
Q

What is the pre-malignant lesion for squamous cell skin cancer?

A

Actinic keratosis

154
Q

A benign capillary hemanioma of infancy that appears in the first few weeks, grows rapidly and then spontaneously regresses is characteristic of?

A

Strawberry hemangioma.

155
Q

What is the name of the target-like lesion that can be caused by HSV?

A

Erythema multiforme

156
Q

Describe toxic epidermal necrolysis

A

It is a drug induced condition and represents the most serious skin hypersensitivity rxn. Usually 30-100% of body surface is affected and Nikolsky sign is positive.

157
Q

What are the reversible signs of cell injury?

A
  • Cellular and mitochondrial swelling
  • Membrane blebbing
  • Nuclear chromatin clumping
  • Ribosomal detachment
158
Q

What are the irreversible signs of cell injury?

A
  • Rupture of lysosomes and autolysis
  • Plasma membrane damage
  • Increased mitochondrial permeability
  • Nuclear pyknosis (condensation)
  • Nuclear karyorrhexis (fragmentation)
  • Nuclear karyolysis (fading)
159
Q

How does tamoxifen interact w/ the endometrium?

A

Unfortunately it can interact with receptors there in an activating manner and it can lead to hyperplasia and increase the risk for endometrial carcinoma.

160
Q

What kind of drug is tamsulosin?

A

It is an alpha 1 adrenergic antagonist. It can be used to tx BPH.

161
Q

What is over-expressed in Burkitt lymphoma?

A

C-MYC

162
Q

What is over-expressed in follicular lymphoma?

A

Bcl-2

163
Q

Which malignancy are pts w/ Trisomy 21 at increased risk for?

A

ALL risk is increased 10-20 fold. AML risk increases too.

164
Q

How does estrogen help maintain bone density?

A

It induces production of osteoprotegrin and decreases expression of RANK on osteoclast progenitor cells.

165
Q

Why does lactate dehydrogenase deficiency cause muscle fatigue and exercise intolerance?

A

Because you need NADH in order to perform glycolysis and if you can’t go through anaerobic respiration you can’t regenerate NADH and thus glycolysis will be prevented from occurring.

166
Q

Where do gummas occur? What is a gumma?

A

They are most commonly cutaneous but can occur elsewhere like subQ tissue, bone, liver, etc.

A gumma is a necrotizing granuloma.

167
Q

What is CD14 a surface marker for?

A

The monocyte-macrophage cell lineage

168
Q

Continued bleeding after Pringle maneuver suggests injury where?

A

Likely hepatic veins or the IVC

169
Q

What is the pathophysiological mechanism of Zenker diverticulum formation?

A

Abnormal spasm or diminished relaxation of the cricopharyngeal muscles during swallowing is thought to be the mechanism. Produces dysphagia. The increased intraluminal pressure eventually results in herniation of the pharyngeal mucosa through a zone of muscle weakness in the posterior pharynx (Killian triangle).

170
Q

Name 2 true and 2 false diverticula

A

True –> appendix and meckel diveriticulum

False –> Zenker diverticulum and diverticulosis.

171
Q

What is meant by the term myocardial hibernation?

A

It refers to a state of chronic myocardial ischemia where myocardial function and metabolism are reduced to match concomitant reduction in coronary blood flow. It leads to systolic dysfunction and is at least partially reversible following re-perfusion.

172
Q

What part of the ECG rhythm strip do B blockers prolong

A

PR interval b/c they slow AV nodal conduction.

173
Q

What are the most common mutations in Lynch syndrome (a disorder where there is mismatch repair mutation)

A

MSH2 and MLH1 which code for components of the MutS and MutL homologs. Mutations to these account for around 90% of cases.

174
Q

What mediates the side effect of flushing, warmth and itching seen w/ niacin?

A

Mainly prostaglandins. Why giving aspirin 30-60 minutes before taking niacin can significantly reduce these side effects

175
Q

What is the mechanism of action of mifepristone?

A

It is a progesterone antagonist that is used in first trimester pregnancy to prevent uterine decidua development and instead there is necrosis leading to abortion.

176
Q

What is the mechanism of action of misoprostol?

A

It is a prostaglandin agonist (PGE1) that causes uterine contractions and leads to expulsion of the pregnancy –> use as part of the mifepristone/misoprostol abortofacient regimen.

177
Q

What secretes somatostatin and what does it do?

A

Somatostatin is secreted by pancreatic delta cells. It decreases the secretion of secretin, CCK, glucagon, insulin and gastrin. It also decreases secretion of GH from the pituitary.

178
Q

What are the glomerular histology characteristics of post streptococcal glomerulonephritis?

A

IF –> C3 granular staining along glomerular BM

Electron microscopy –> subepithelial humps

179
Q

What are the glomerular histology characteristics of IgA nephropathy?

A

Light microscopy –> mesangial hypercellularity

IF –> IgA in the mesangium

180
Q

What are the glomerular histology characteristics of Alport syndrome?

A

Electron microscopy –> lamellated appearance of the glomerular basement membrane

181
Q

What is Henloch-Schonlein purpura?

A

IgA nephropathy w/ extrarenal sxs like abdominal pain, arthralgias, and purpuric skin lesions.

182
Q

What encapsulates the cystic cavities formed by ischemic brain infarcts?

A

Dense fibers formed by astrocytic processes.

183
Q

What are acrochordons?

A

Skin tags (pedunculated outgrowths of normal skin)

184
Q

Which cholinesterase inhibitors can cross the BBB and which cannot?

A

Can cross –> the tertiary amines as they are lipophilic. These include physostigmine, galantamine, donepezil, and rivastigmine.

Cannot cross –> the quaternary amines as they are hydrophilic. These include neostigmine, edrophonium and pyridostigmine.

185
Q

How do chronically elevated free fatty acids contribute to disease pathogenesis in T2DM?

A

FFAs contribute to insulin resistance by impairing insulin-dependent glucose uptake and increasing hepatic gluconeogenesis.

186
Q

The azurophilic granules in APML stain positive for what?

A

Myeloperoxidase.

Note that auer rods are deformed azurophilic granules

187
Q

Which malignancy stains positive for tartrate resistant acid phosphatase (TRAP)?

A

Hairy cell leukemia

188
Q

What is a distinguishing characteristic btwn dysplasia and carcinoma?

A

Dysplasia is a reversible process that precedes carcinoma development. Once you arrive at carcinoma you can’t go back.

189
Q

What causes the interstitial and alveolar edema and exudate in ARDS?

A

Increased pulmonary capillary permeability

190
Q

What is the mechanism of digoxin decreasing the ventricular rate when used in afib?

A

It increases parasympathetic tone, which leads to inhibition of AV nodal conduction.

191
Q

How does the calcium-calmodulin complex lead to smooth muscle contraction?

A

It activates myosin light chain kinase (MLCK) which in turn phosphorylates myosin light chains. This will facilitate cross bridge formation and smooth muscle contraction.

192
Q

Is joint involvement typically symmetric or asymmetric is psoriatic arthritis?

A

More than 50% of pts have asymmetric involvement.

193
Q

What is the most common defect in leukocyte adhesion deficiency?

A

It is most commonly due to defect of integrins. Note that it is integrins on the leukocytes interacting with CAMs on the endothelium.

194
Q

What is a cystocele and how does it present?

A

A cystocele (aka anterior prolapse) is where the bladder bulges into the vagina. This is due to supportive tissue between vaginal wall and bladder weakening and stretching. It presents w/ bulge of the anterior vaginal wall on valsalva.

195
Q

What are the branchial pouches derived from?

A

Endoderm. Note that this is different than the branchial arches which are derived from mesoderm and neural crest tissue.

196
Q

What is Osler-Weber-Rendu syndrome? How does it present?

A

It is an autosomal dominant inherited disease of blood vessels. It is also called hereditary hemorrhagic talengiectasia. Presents w/ branching skin lesions (telangiectasias), recurrent epistaxis, skin discolorations, arteriovenous malformations (AVMs), GI bleeding, hematuria.

This one had those weird tongue lesions on form 18

197
Q

What is the equation for calculating LDL?

A

LDL = total cholesterol - (HDL + TG/5)

*I’m pretty sure this is b/c VLDL = TG/5 roughly

198
Q

What is the strongest triglyceride lowering agent?

A

Fibrates! Statins and niacin lower it some but fibrates are by far the best at this.

199
Q

What sort of drug is colestipol? What does it do and name other drugs in this category?

A

It is a bile acid resin like cholestyramine and coleselevam. It works by preventing the reabsorption of bile acids and this lowers LDL while raising HDL and TG slightly.

200
Q

How does orlistat work?

A

It inhibits gastric and pancreatic lipase. This effect is used clinically for weight loss.

201
Q

What is a cardiac complication of long term obstructive lung disease?

A

Cor pulmonale caused by chronic hypoxic vasoconstriction (i.e. person w/ COPD from 100 pack year smoking hx can get isolated R heart failure).

202
Q

What is the pathophysiology of gynecomastia in liver failure? What is another way it can occur in men?

A

Failure of the liver to degrade estrogen.

Per First Aid, gynecomastia can also occur in men when there is increased androgen binding protein leading to decreased free testosterone this can also cause it.

203
Q

In what way is the level of potassium altered in bulimia nervosa?

A

K+ levels go down (loss in vomitus/saliva I believe)

204
Q

What sort of arthropod is Ixodes?

A

It is a tick!

205
Q

What can RBCs show inside them on blood smear in babesiosis?

A

Intraerythrocytic rings and maltese cross formations

206
Q

What is cyclosporin used for? What’s its mechanism of action? What are its ADRs?

A

It is an immunosuppressant that inhibits calcineurin by binding cyclophilin and this blocks T-cell activation by preventing IL-2 transcription.

Major ADRs include nephrotoxicity (this is the big one I think), HTN, hyperlipidemia, neurotoxicity, gingival hyperplasia and hirsutism.

207
Q

What nerve innervates triceps brachii?

A

Radial nerve. This is why injury to the nerve at the radial groove causes weakness of elbow extension.

208
Q

How does histone methylation affect DNA? What about histone acetylation?

A

Histone methylation usually represses DNA transcription. Note that it can promote it in some circumstances.

Acetylation of histones relaxes DNA coiling allowing for transcription.

209
Q

How does CpG methylation of DNA affect it?

A

It represses transcription.

210
Q

How does tx of APML w/ all-trans retinoic acid have a therapeutic effect?

A

It induced differentiation of pro-myelocytes.

211
Q

True or false, adenosine is one of the factors important for autoregulation of blood flow at the heart?

A

True!

212
Q

When is liquefactive necrosis seen?

A

In bacterial abscesses and brain infarcts

213
Q

When is caseous necrosis seen?

A

Stuff like TB and systemic fungi –> macrophages wall off the offending organism. There can be granular debris.

214
Q

When is fat necrosis seen?

A

It is the result of damaged cells releasing lipase which leads to enzymatic digestion of fat cells. Can be seen in acute pancreatitis and fat necrosis after breast trauma.

215
Q

When is coagulative necrosis seen?

A

Ischemia/infarcts of most tissue except for brain

216
Q

When is fibrinoid necrosis seen?

A

In immune reactions with vessels –> immune complexes combine w/ fibrin

217
Q

What is the rxn that statins inhibit?

A

They inhibit the conversion of HMG CoA to mevalonate

218
Q

In which CAH is 17-hydroxyprogesterone elevated?

A

21-hydroxylase deficiency

219
Q

What sort of tx should a patient who is dx w/ Kaposi’s sarcoma receive?

A

HAART therapy to tx HIV and anti-neoplastic therapy to tx the malignancy

220
Q

What are the two substrates at the start of the heme synthesis pathway?

A

Succinyl CoA and glycine

221
Q

What is the murmur of mitral stenosis?

A

A mid-diastolic low-pitching rumbling murmur that is heard best at the apex w/ the pt lying in L lateral decubitus.

222
Q

What is mutated in Peutz-Jeghers syndrome?

A

Autosomal dominant condition due to STK11 gene mutation on chromosome 19

223
Q

Granular deposition of IgA in the upper papillary dermis is characteristic of what?

A

Dermatitis herpetiformis

224
Q

What does the otic ganglion innervate?

A

The parotid gland for salivation.

225
Q

Where do pre-ganglionic parasympathetics from the edinger westphal nucleus go?

A

To the ciliary ganglion. They synapse and then the post-ganglionic fibers (in the form of short ciliary nerves) innervate sphincter pupillae and ciliaris muscles.

226
Q

What is one way that long term EtOH abuse can affect the cerebellum?

A

Can lead to alcoholic cerebellar degeneration, which is most pronounced in the vermis.

227
Q

In Wernicke-Korsakoff syndrome there are lesions to…?

A

The mammillary bodies and the anterior and medial thalami.

228
Q

Absence of tonsils on PE is indicative of what primary immunodeficiency?

A

X-linked agammaglobulinemia. No B cell development so no lymphoid tissue.

229
Q

What does mutation to TP53 cause?

A

Li-Fraumeni syndrome (sarcoma, breast, adrenal gland and leukemia cancers)

230
Q

Which class of immunosuppressants cause afferent and efferent renal arteriole constriction leading to a dose-dependent rise in BUN and creatinine?

A

Calcineurin inhibitors like tacrolimus and cyclosporin

231
Q

How does tissue ischemia affect ion concentrations? Why?

A

Tissues ischemia means cells lack the ATP to maintain the Na/K ATPase pump that maintains ion concentration gradients. As such, there is increased Na+ entry into cells and there is more K+ efflux than normal, resulting in an increased extracellular K+ concentration.

Overall, increased extracellular K+ occurs and there can also be reduced Na+, HCO3- and Ca++ extracellularly. Increased cytoplasmic concentration of Ca++ is a hallmark of ischemic injury.

232
Q

What are the three stimuli of JG cell release of renin?

A

Decreased NaCl sensed by the macula densa, decreased pressure in the afferent arteriole, and sympathetic stimulation.

233
Q

What makes up hyaline casts (can be seen in pre-renal azotemia)? Where does it come from?

A

Hyaline casts are made up of Tamm-Horsfall protein, which is a glycoprotein secreted by renal tubular epithelial cells of the ascending loop of Henle.

234
Q

What is the foam stability index test?

A

Where you add amniotic fluid to wells containing ethanol, shake and evaluate for the formation of rings. It is a test for fetal lung maturity.

235
Q

What is a pancreatic pseudocyst?

A

A collection of fluid, pancreatic enzymes and blood that is surrounded by fibrous tissue. Occurs in the setting of pancreatitis.

236
Q

What property makes heparin better for use in pregnancy than warfarin?

A

Heparin is water soluble so it does not cross the placenta. Warfarin is lipophilic and as such can cross the placenta and have teratogenic effects.

237
Q

CMV retinitis classically affects pts w/ a CD4 count of?

A

Less than 50

238
Q

What is the mechanism of action of gancyclovir?

A

Inhibits viral DNA replication by incorporating into viral DNA.

239
Q

What causes the proptosis/exophthalmos seen in Graves disease?

A

Glycosaminoglycan accumulation in retro-orbital tissue due to stimulation of orbital fibroblasts.

240
Q

Which jugular venous tracing wave is absent in afib?

A

The a wave (first one) as this represents atrial contraction.

241
Q

What are the 5 cyanotic congenital heart conditions?

A
  • Tetralogy of fallot (most common)
  • Truncus arteriosus
  • Tricuspid atresia
  • Transposition of the great arteries
  • Totally anomalous pulmonary venous connection
242
Q

Where are the stem cells for the intestinal epithelium?

A

In the crypts. They are called the crypts of Lieberkuhn.

243
Q

What is the primary cell type w/in the nodules of hepatic cirrhosis?

A

hepatocytes. The nodules are separated by bridging fibrous septae.

244
Q

What is the pathophysiology of lactose intolerance in most cases?

A

In most cases it due to decreased gene expression. In most ethnicities, the expression of lactase decreases with age.

245
Q

What is the most important RF for a primary thyroid malignancy?

A

Radiation exposure. This is because the thyroid gland is the most radiation-sensitive tissue in the body.

246
Q

What is the equation for ventilation?

A

TV x RR = ventilation

247
Q

What is the mechanism of action of anakinra?

A

It is an IL-1 receptor blocker

248
Q

What is the mechanism of action of sirolimus?

A

It is an immunosuppressant that works by blocking mTOR. This blocks T cell activation and B cell differentiation by preventing a response to IL-2.

249
Q

What is mycophenolate mofetil?

A

It’s an immunosuppressant that interrupts purine synthesis of T and B cells.

250
Q

What are Negri bodies?

A

They are eosinophilic cytoplasmic inclusions that can be seen on brain histopathology in Rabies infection.