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Step 1 Miscellanous > Rote Memorization Factoids > Flashcards

Rote Memorization Factoids Flashcards

1
Q

What trinucleotide repeat causes Huntington disease and what is the mnemonic?

A

CAG
Caudate has decreased
ACh
GABA

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2
Q

What trinucleotide repeat causes myotonic dystrophy and what is the mnemonic?

A

CTG
Cataracts
Toupee
Gonadal atrophy

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3
Q

What trinucleotide repeat causes Fragile X syndrome and what is the mnemonic?

A

CGG
Chin
Giant
Gonads

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4
Q

What trinucleotide repeat causes Friedreich ataxia and what is the mnemonic?

A

GAA

Ataxic GAAit

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5
Q

What bone abnormality is common in Down syndrome patients?

A

Hypoplastic nasal bone

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6
Q

How do you tell Edwards syndrome and Down syndrome apart via Quad screen?

A

Down syndrome: decreased aFP, INCREASED B-hCG, decreased estriol, INCREASED inhibin A

Edwards syndrome: decreased aFP, DECREASED B-hCG, decreased estriol, DECREASED or NORMAL inhibin A

Down syndrome is only one where Beta-HCG will be increased

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7
Q

What chromosome is associated with Wilson disease?

A

13 - so unlucky he lost his ball

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8
Q

What chromosome is associated with NF-1?

A

17 - von Recklinghaus

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9
Q

What chromosome is associated with BRCA1 and Li Fraumeni?

A

17

Li Fraumeni = p53
Same chromosome as NF-1

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10
Q

What chromosome is associated with ADPKD 1?

A

16 - same as alpha thalassemia

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11
Q

What chromosome is associated with ADPKD2?

A

4 - same as Huntington

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12
Q

What chromosome is associated with achondroplasia?

A

4

FGF3, baby is wee

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13
Q

What chromosome is associated with Friedrich ataxia?

A

9 - memorize the slide

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14
Q

What chromosome is associated with Wilms tumor?

A

11

Remember, Beckwith-Wiedmann is 11p15 and is associated

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15
Q

What chromosome is associated with beta-globulin defects?

A

11

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16
Q

What chromosome is associated with Rb1 and BRCA2?

A

13 - same as Patau

Remember that BRCA1 and p53 are associated on the same chromosome as NF-1

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17
Q

What chromosome is associated with alpha-globulin defects?

A

16, 6 looks like a backwards a

Same as ADPKD

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18
Q

What chromosome is associated with hemochromatosis?

A

6

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19
Q

What chromosome is associated with both Cri-du-chat and familial adenomatous polyposis (FAP)?

A

5

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20
Q

What chromosome is associated with Huntington disease?

A

4, same as ADPKD2 and achondroplasia

Hunting 4 Food

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21
Q

What chromosome is associated with cystic fibrosis and Williams syndrome?

A

7 (10 less than NF-1)

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22
Q

What chromosome is associated with von Hippel-Lindau disease and renal cell carcinoma?

A

Chromosome 3 (3 letters)

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23
Q

What is the Rheumatoid factor antibody targeted against in Rheumatoid arthritis? What type of Ab is it?

A

IgM antibody targeted against Fc region on IgG

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24
Q

What two nucleotides are at the 5’ and 3’ ends of a splice site?

A

5’ end - donor side - GU
3’ end - acceptor side - AG

Donor side will attack middle to form a lariat (looped intermediate), then 3’ hydroxyl of 5’ side of intron will attack the phosphodiester bond between G and the exon to splice out the intron. This whole process is mediated by snRNPs.

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25
Q

What tumor is associated with pure red cell aplasia (isolated anemia with lack of reticulocytes)? What virus is?

A

Thymoma - one of the paraneoplastic syndromes.

Thymoma is also associated with myasthenia gravis

-> virus is Parvovirus B19 (aplastic anemia due to anti-B19 antibodies)

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26
Q

What is Stewart Treves syndrome?

A

Angiosarcoma arising in the setting of chronic post-mastectomy lymphedema

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27
Q

What is Uhthoff’s phenomenon?

A

Tendency of demyelinating diseases to worsen when exposed to exercise and hot temperatures because nerve conduction does not work properly at higher temperatures
-> reason why optic neuritis and neural symptoms tend to worsen when patients with MS exercise or go in saunas

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28
Q

What are the causes of hyperuricemia due to overproduction?

A

HGPRT deficiency (Lesch-Nyhan)
PRPP synthetase overactivity
G6PD deficiency
Myeloproliferative disorders -> i.e. polycythemia vera
Cytotoxic chemotherapy, sickle cell anemia -> which lead to increased cell turnover

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29
Q

What is somatomedin C?

A

IGF-1 - “mediates” your growth

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30
Q

What antibody is associated with autoimmune hepatitis?

A

Anti-Smooth Muscle. Also anti-liver microsomal Ab

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31
Q

What antibody is especially associated with polymyositis / dermatomyositis?

A

Anti-Jo-1, which is an anti-histidyl-tRNA synthetase
(attaches histidine to tRNA)

ANA (like lupus) may also be positive in dermatomyositis but is less specific

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32
Q

What’s the first line treatment for hypertriglyceridemia?

A

Fibrates - i.e. gemfibrozil, fenofibrate

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33
Q

What’s the use of niacin?

A

Mainly to raise HDL levels. Also a modest reduction of triglycerides (like fibrates)

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34
Q

What is the formula for drug clearance with respect to first order drug elimination?

A

“cde”

Clearance = volume of Distribution * Elimination constant

CL = Vd * Ke

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35
Q

What is the formula for elimination constant?

A

Ke = 0.7 / (t1/2)

Elimination constant = 0.7 / (half life)

Units are time^-1

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36
Q

What is the steady state equation?

A

input = output

f(D/T) = (C_ss)(CL)
concentration/time = (concentration/volume)(volume/time)

Where C_ss = Concentration at steady state (plasma drug concentration)
f = bioavailability, which is 1 for IV administration. Decreases with first pass metabolism / incomplete absorption.

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37
Q

What is the formula for loading dose?

A

Vd * Css

Volume of distribution time concentration at steady state

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38
Q

What is the formula for maintenance dose?

A

Dose maintenance = Css * CL, the output side of the steady state equation.

Dose maintenance is thus essentially equal to f(D/T), as its units are amount per time. We are usually giving the drug IV as well so f = 1, so it’s just D/T.

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39
Q

What is filtration fraction?

A

FF = GFR / RPF

Renal plasma flow = Renal blood flow (RBF) * (1 - hematocrit)

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40
Q

How do you approximate GFR and RPF?

A

GFR = Clearance of creatinine (slightly overpredicts because it is secreted sightly) or clearance of inulin

RPF = Clearance of PAH (roughly. Really calculating effective renal plasma flow / eRPF, which slightly underestimates the truth)

Clearance of X = Urinary concentration of X * Urine flow rate (V) / Plasma concentration of X

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41
Q

What is used as a marker for Mast cell activation? What else is released by mast cells?

A

TryptASE (not trypsin)

Also released by mast cells -> heparin (keeps blood flow), histamine, eosinophilic chemotactic factor (brings in eos), and leukotrienes

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42
Q

What is the function of tryptase?

A

Marker of mast cells

Importantly:
also used in Club / clara cells to possibly cleave hemagglutinin to allow activation of the flu virus in the respiratory system.

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43
Q

What is the order of frequency of vessels involved in atherosclerosis?

A

445

Abdominal aorta (large elastic arteries most likely) > coronary arteries > popliteal arteries > carotid arteries (branch point of carotid sinus)

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44
Q

What’s the antidote for cholinesterase poisoning?

A

Atropine (ACh competitive antagonist) + pralidoxime (also will have an effect on nicotinic junctions once it inactivates the organophosphate)

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45
Q

What gene is wrong in hemochromatosis and what does this cause?

A

HFE gene - C282Y allele most common (recessive)

Increased Divalent metal cation transporter (DMT1)
Decreased hepcidin production -> increased circulating iron

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46
Q

What protein mediates the cell surface adhesion of the paramyxoviruses?

A

Hemagglutinin - like influenza, think of the octopus dishes in the scene, and the three wolves outside for parainfluenza virus (represents possessing all three major virulence proteins, including fusion protein, hemagglutinin, and neuraminidase)

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47
Q

What two neurologic conditions are associated with high arch / instep?

A
  1. Charcot Marie Tooth Disease - Hereditary Motor and Sensory Neuropathy
  2. Friedreich Ataxia
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48
Q

What marker is used for disease monitoring in sarcoidosis?

A

ACE levels

-> produced by the macrophages in the periphery of the granulomas

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49
Q

What receptor does Parvovirus B19 attach with?

A

P antigen on RBCs, also know as globoside

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50
Q

What is the most common variant of cystic fibrosis?

A

The deltaF508 mutation where the phenylalanine is lost which causes improper folding and glycosylation (post-translational modification) of the CFTR, leading to targeting of the protein for proteasomal degradation.

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51
Q

What age group typically gets HUS?

A

Children under age 10

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52
Q

Where does benzene come from and what does it predispose you to?

A

Comes from tobacco smoke, gasoline fumes, and industrial processes

Predisposes to aplastic anemia, AML, and myelodysplastic syndromes

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53
Q

Other than endometriosis, what is the other indication for danazol?

A

Hereditary angioedema

-> increases complement C4 and C1 inhibitor production by unknown mechanisms

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54
Q

What’s the mechanism of action of cyproterone?

A

Androgen receptor antagonist

- pg. 620

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55
Q

What vitamin do exclusively breast-fed infants require which formula fed infants do not?

A

Vitamin D, especially if the baby is darkskinned

Formula is fortified with enough vitamin D to make this not an issue. Vitamin D and Vitamin K are not present in high amounts in the breast milk.

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56
Q

What are lipoxins?

A

A product made from leukotrienes within platelets which are inhibitory to acute inflammation

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57
Q

What lines define the boundaries of the sarcomere? What is directly in the center?

A

Z lines - where the actin bands attach

Directly in the center - M line, where myosin bands attach

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58
Q

What is the line between ends of the light bands called?

A

H bands

LIght bands are composed of actin and make up the I bands
dArk bands are composed of myosin and make up the A bands

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59
Q

What is the mechanism of action of Staphylococcal Toxic Shock Syndrome Toxin (TSST) causing toxic shock?

A

Superantigen which binds MHC II of APCs (i.e. macrophages / dendritic cells) to the T cell receptor of CD4 cells

  • > CD4 cells will release IL-2
  • > Macrophages will release TNFalpha and IL-1, mediating toxic shock
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60
Q

What organism causes hydatid cysts in the liver?

A

Echinococcus granulosus - #61

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61
Q

What is the most common site of osteomyelitis in adults and the most sensitive way of imaging this?

A

Vertebral column

Most sensitive way of imaging = MRI

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62
Q

Patient has severe watery diarrhea (rice-water stools) and odor of garlic on breath after consuming insecticide. What are they poisoned with and what is the treatment? What cardiac manifestation is possible from this poisoning?

A

Arsenic - Dimercaprol

- possible QT prolongation -> torsades

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63
Q

What does the breath of someone who ingested cyanide smell like?

A

Bitter almonds

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64
Q

What is the function of phospholipids / lecithin in bile?

A

Works in conjunction with bile salts to solubilize cholesterol and prevent stone formation
-> will be low in people with gallstones

Makes sense because phospholipids are ampipathic (They are a component of membranes), so they would help solubilize

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65
Q

What vitamins will be increased vs decreased in small intestinal bacterial overgrowth?

A

Increased - Vitamin K, folate (produced by intestinal bacteria)

Decreased - All the rest

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66
Q

What does tracheal deviation towards the side of a radioopaque CXR likely mean?

A

Atelectasis caused by bronchial obstruction (with gradual resorption of air distal to the block)
-> loss of radiolucent air and filling of the hemithorax with other material causes it to become radioopaque (vs mneumothorax)

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67
Q

What cancers are associated with paraneoplastic cerebellar degeneration? What are the antibodies which cause this?

A

Present with ataxia:

Gynecologic / breast cancers - anti-Yo
“Ay-YO babygirl, u making me swoon and fall over”

Small cell lung cancer - anti-Hu
“Small Hu-man” -> also causes paraneoplastic encephalomyelitis, so just many antibodies against brain

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68
Q

Why do tumor cells have prominent nucleoli?

A

Upregulation of rRNA synthesis (occurs in nucleoli) in order to synthesize proteins faster, for rapid cell turnover

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69
Q

What is the only rRNA component to be made outside of the nucleolus and what makes it?

A

5S rRNA, a component of the 60S ribosome.

Made inside the nucleus but outside the nucleolus by RNA polymerase III

All other rRNA is synthesized by RNA polymerase I inside the nucleolus.
#2039
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70
Q

Is procollagen peptidase present in the intracellular or extracellular space? What disease does it cause if it’s absent?

A

Present extracellularly, cleaves the N/C terminals of procollagen to tropocollagen, which can form staggered tropocollagen ready to be cross-linked

Deficiency = Ehlers-Danlos. This is one variant

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71
Q

What is accumulating in basophilic stippling?

A

Residual ribosomes

NOT iron-laden mitochondria (as in ringed sideroblasts in the bone marrow)

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72
Q

What infection does secondhand smoke greatly increase your risk for?

A

Otitis media - #310

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73
Q

What protein do integrins bind in the basement membrane?

A

Fibronectin - #1872

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74
Q

What urinary osmolality indicates probably SIADH in the setting of hyponatremia and decreased plasma osmolality?

A

> 100 mOsm/kg H20

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75
Q

What is an idiosyncratic drug reaction? Give an example.

A

A drug reaction due to complex genetic or metabolic differences between patients (i.e. G6PD deficiency, fast or slow acetylators, etc)
Called idiosyncratic because everyone has their idiosyncracies.

i.e. A patient given primaquine has hemolytic anemia due to G6PD deficiency.

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76
Q

What is the signal transducer of the protein kinase B pathway (Akt)? Its funciton?

A

Pi3k -> Akt -> mTOR

mTOR translocates to the nucleus and controls cell growth

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77
Q

What is the inhibitor of the Pi3K/mTOR pathway?

A

PTEN - tumor suppressor gene. Will dephosphorylate the PIP3 which is the product of Pi3k.

Remember this is the same tumor suppressor mutated in endometrial hyperplasia

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78
Q

What is disopyramide vs dipyridamole?

A

Disopyramide - Disappears! class 1A antiarrhythmic

Dipyridamole - coronary steal phosphodiesterase inhibitor

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79
Q

What other marker is used in conjunction with AFP (alpha fetoprotein) for the detection of neural tube defects in utero?

A 
AChE - Acetylcholinesterase
#502
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80
Q

What is phlegmasia alba dolens?

A

Painful white “milk leg”
-> complete occlusion of a deep leg vein (i.e. femoral) -> leads to blockade of arterial flow
-> blood flows thru superficial system instead
#474
-> next step would be occlusion of superficial system and total whiteness

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81
Q

What is dornase alfa and what condition is it used in?

A

Recombinant DNAse -> used in CF to thin out mucosal secretions

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82
Q

What drug slows disease progression in CF, and what antibiotic is typically used as an anti-inflammatory agent?

A

Ibuprofen actually slows disease progress -> prevents inflammation / airway destruction

Azithromycin is used as an antiinflammatory

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83
Q

What divalent anion do cadherins require to maintain the adherens junction between epithelial cells?

A 
Calcium
#6502
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84
Q

Does kidney function return to 100% after 1 kidney is removed?

A 
No -> will gradually rise to 80% of normal with compensatory changes
#6555
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85
Q

Why would using an alkaline growth medium reduce antibiotic resistance in some bacteria?

A 
H+ gradient generated by bacterial electron transport chains pumps protons out. This extracellular acidity is required for production of ATP, and operation of multidrug efflux pumps
#6526
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86
Q

What’s the breakdown pathway of NE / E?

A

NE -> normetanephrine, via COMT
E -> metanephrine, via COMT

Normetanephrine and metanephrine -> vanillylmandelic acid (VMA) via MAO.

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87
Q

What is the most significant risk factor the for the development of osteoarthritis?

A

AGE!

Not weight-bearing exercise, tho it's important
#6450
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88
Q

What is Chlorpropamide vs Chlorthalidone vs Chlorpromazine vs Thioridazine?

A

Chlorpropamide - 1st generation sulfonylurea

Chlorthalidone - Long acting thiazide diuretic

Chlorpromazine - Low potency 1st generation antipsychotic associated with Corneal deposits

Thioridazine - Low potency 1st generation antipsychotic associated with reTinal deposits

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89
Q

How does protein synthesis during apoptosis continue when there is a lack of initiation factors?

A

Ribosomes begin binding to a special site in the 5’-UTR of the mRNA called the Internal Ribosome Entry Site (IRES)

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90
Q

How do you tell apart neuropathic vs venous vs arterial ulcers in diabetic patients?

A

6498

Arterial ulcers - tend to appear on distal digits (farthest from the blood supply) -> secondary to atherosclerosis. Very painful.

Venous - tend to arise on shins / medial malleous, along with stasis dermatitis -> secondary to venous stasis / vascular insufficiency.

Neuropathic ulcers - tend to arise on bony prominences and present without pain -> no pain b/c nerves are not there. Bony prominences are the inciting trauma.

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91
Q

What is agrammatism?

A

The characteristic speech pattern in Broca’s aphasia, where nouns and verbs are all that remains.

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92
Q

Is speech in Broca’s aphasia slurred?

A

No - slurring of speech = dysarthria -> motor inability to speak (i.e. due to knockout of area 4).

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93
Q

What is aphasia?

A

A higher-order language deficit in general

-> i.e. Broca, Wernicke, Global, etc

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94
Q

What type of nerve innervates postganglionic autonomics?

A

Unmyelinated, C fibers

Same as those controlling slow, onset, dull visceral pain (free nerve endings)

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95
Q

What type of nerve innervates preganglionic autonomics?

A

Lightly myelinated, B fibers

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96
Q

What is one key clinical finding which can differentiate between reactive arthritis and disseminated gonoccal infection (gonococcal arthritis)?

A

Gonococcal arthritis lacks any eye findings

Reactive arthritis causes uveitis

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97
Q

What is a tyloma and what causes it?

A 
Skin callus - painless thickening of stratum corneum occurs at areas of repeated trauma, especially palms and soles (thick skin)
#6451
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98
Q

What drug should be used to prevent thromboembolism in patients with prosthetic valves?

A

Warfarin

-> remember, clopidogrel and abciximab are used in acute coronary syndromes

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99
Q

What is the course of the PCA and what type of herniation does it get injured in?

A

Courses laterally around crus cerebri, then on the inferior / medial surface of the temporal and occipital lobes

  • > as it is present on the medial surface of the temporal lobe, uncal herniation will lead to compression of the ipsilateral PCA with nearby brain.
  • > contralateral homonymous hemianopsia.
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100
Q

What GHRH analog is used to treat HIV-associated lipodystrophy?

A

Tesamorelin

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101
Q

What factors utilize a nonreceptor tyrosine kinase? (i.e. JAK/STAT)?

A

Prolactin, GH (jak and the beanstalk), cytokines, and hematopoietic growth factors

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102
Q

What factors utilize a receptor tyrosine kinase?

A

Insulin, IGF-1, FGF, PDGF, EGF

-> think growth factors, and insulin is really a type of growth factor

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103
Q

What receptor type do FSH, LH, ACTH, TSH, CRH, and hCG use?

A

Gs -> cAMP

104
Q

What receptor type do GnRH, Oxytocin, and Gastrin use?

A

Gq -> remember it signals thru IP3 just like the M3 receptor

105
Q

What secretes GIP and what is its function?

A

K cells (duodenum / jejunum), in response to food.

Gastric inhibitory peptide -> inhibits H+ secretion, also increases insulin release (an incretin)

106
Q

What is the most prominent function of VIP and what stimulates / inhibits it?

A

Present in the parasympathetic ganglia of the sphincters -> works as an inhibitor transmitter (with NO) to allow opening of LES

Stimulates by distention / vagal stimulation (pro-food), inhibited by adrenergic input (anti-food)

107
Q

What does a VIPoma do and why?

A

Watery diarrhea, hypokalemia, achlorhydria

  • > “pancreatic cholera”
  • > in addition to being necessary for relaxation, it also DECREASES gastric acid secretion, and greatly increases electrolyte secretion by pancreatic ducts (“VASOACTIVE”).
  • > improves intestinal motility with secretions
108
Q

What controls ghrelin secretion / how does this work? Will it be increased or decreased in gastric bypass surgery?

A

Lack of stomach distension -> ghrelin release (hunger). Released by stomach, increases appetite by acting on arcuate nucleus to increased AGrP / NPY signalling to lateral hypothalamus to increase hunger.

Decreased by gastric bypass (increased satiety)

109
Q

How does the D-xylose absorption test work? What is it testing for?

A

D-xylose does not require pancreatic enzymes for uptake

  • > should be detectable in serum if GI mucosa is intact
  • > can distinguish from other forms of malabsorption
110
Q

What is the primary test used for pancreatic function testing?

A

Secretin test -> see if pancreatic secretions increase with secretin.
-> cumbersome to do. Usually just do a trial of pancreatic enzyme if you see there is malabsorption (i.e. Sudan fecal testing shows fat in the stool)

111
Q

What is the order of sites of fetal hematopoiesis?

A

Yolk Sac
Liver
Spleen
Bone Marrow

Young Liver Synthesizes Blood

112
Q

What property of fetal hemoglobin increases its affinity for oxygen?

A

Less avid binding of 2,3-BPG.

113
Q

What type of patient usually gives ABO hemolytic disease of the newborn?

A

A type O mom, who manages to form anti-A or anti-B IgG antibodies somehow -> tends to be milder than Rh hemolytic disease of the newborn

114
Q

Is hemoglobin positively / negatively charged which affects its migration?

A

Negatively! Thus migrates towards the positively charged anode.
-> just remember anode attracts the negatives

Explains why things which increase positive charge (i.e. glutamate -> lysine) in hemoglobin C -> decrease migrations.

115
Q

Do dense granules appear light or dark on EM? What do they contain?

A 
Dense - dark - delta granules
-> contain ASC:
ADP
Serotonin
Ca+2
116
Q

What does ristocetin do?

A

Activates vWF factor (released by alpha granules of platelets and WP bodies) to bind Gp1b

-> defective in von Willebrand disease and Bernard-Soulier

117
Q

What are T-tubules and terminal cisternae?

A

T-tubules - Transverse tubules, invagination of the plasma membrane

Terminal cisternae - continuations of the sarcoplasmic reticulum

118
Q

What pattern do T tubules + terminal cisternae form in skeletal muscle and where are they?

A 
Form triads (One T tubule, two terminal cisternae)
-> At the A/I band junction (2 per sarcomere)
119
Q

What pattern do T tubules + terminal cisternae form in cardiac muscle and where are they?

A 
Form dyads (One T tubule, one terminal cisternae)
-> At the Z line (1 per sarcomere)
120
Q

What is the H band? How does it change with contraction?

A

The space between overlapping A/I binds, centered around the M line

Gets smaller during contraciton

121
Q

What bone formation type makes the clavicle?

A

Intramembranous (same as face)

122
Q

What is the relative potency of the three types of estrogen?

A

Estradiol > estrone > estriol (produced by placenta)

123
Q

What is Mittelschmerz?

A

“Middle hurts” - mid-cycle ovulatory pain due to peritoneal irritation from follicle rupture
-> may mimic appendicitis

124
Q

What is gestational age vs embryonic age?

A

Gestational age - age calculated since last menstrual period

Embryonic age - age calculated from date of conception (gestational age minus 2 weeks)

125
Q

What are four physiologic adaptions that happen during pregnancy?

A
  1. Increased cardiac output -> increased preload, decreased afterload, increased heart rate
  2. Anemia -> due to relative increase in plasma vs RBCs
  3. Hypercoagulability -> Needed to reduce blood loss at delivery
  4. Hyperventilation -> blow off fetal CO2
126
Q

What subunit of HCG is unique?

A

Beta! that’s why we measure beta-HCG

alpha-HCG is homologous to FSH, LH, and TSH

127
Q

What is the most specific marker for menopause?

A

Increased FSH (due to loss of negative feedback on estrogen)

128
Q

What unique morphologic feature helps identify a liposarcoma?

A 
Scalloping / indentation of the nucleus via lipid droplets
#6626
129
Q

Why do children of diabetic mothers have an increased risk of neonatal respiratory distress?

A

Insulin slows lung development.

130
Q

What does free air under the diaphragm often indicate?

A

6683

Bowel perforation -> allows air to leak from the bowel into the peritoneal space. Often happens in cases of ruptured megacolon or ruptured ulcer.

131
Q

What types of things do and do not cross the placenta?

A

Do cross - lipophilic things, i.e. unconjugated bilirubin

Do not cross - hydrophilic things and charged things, i.e. conjugated bilirubin

132
Q

What caused a females infertility if there are no useful clinical findings or clues?

A 
Pelvic inflammatory disease
#6634
133
Q

A red vesicular rash in a streaky pattern is present on the extremities, on the hands and arms, after camping in an area filled with tics. The patient doesn’t have a fever. What is the diagnosis?

A

Allergic contact dermatitis, due to poison ivy.

Rocky mountain spotted fever presents with a PETECHIAL rash with FEVER.
#6652
134
Q

Will urine pH be high or low of it’s acidic.

A

LOW

low pH = acid. You are legit trolling bro

135
Q

What does polyploidy mean?

A

Having more than 2 full sets of chromosomes

136
Q

How does contact inhibition work?

A

Contact inhibition - normal cells will detect nearby cells and bind them via adherens junctions (cadherin / catenin). Binding via Ca+2 dependent cadherins -> sequestration of beta-catenin -> prevention of beta-catenin from going to nucleus and activating gene transcription.

This is a regulatory mechanism for tissue repair and preventing overgrowth of tissues

137
Q

How do cancer cells grow on a Petri dish and why?

A

Loss of contact inhibition -> growth ontop of eachother since they don’t care at all about being in contact -> grow in mounds

Thus, normal cells should only make a thin layer on a Petri dish since they stop growing when in contact with eachother.

138
Q

What is the function of the APC gene?

A

Holds onto Beta-catenin in the cytoplasm to prevent it from moving and initiating cell proliferation. Wnt pathway signalling will cause APC to detach from beta-catenin and increase proliferation.

139
Q

Why are aminoglycosides not used for gram + bacteria? How can you them for this purpose?

A 
They do not penetrate the thick cell wall of gram + bacteria very well
-> can combine with a beta-lactam so they can enter, and will have effective gram + coverage (i.e. enterococcus)
#6748
140
Q

Are neutrophils involved in the response to Chlamydia? How do you see them?

A

Yes -> they can phagocytose the bacteria

They cannot be seen inside via Gram stain due to lack of muramic acid (vs gonococcus), but can be visualized via Giemsa stain.

141
Q

What is the mechanism of cough syncope?

A

Patients with COPD or other conditions can go into coughing fits -> during the strain phase, blood is held in the abdomen and cannot go back to the heart (due to increase intrathoracic pressure)
-> can also happen in a Valsalva manuever
-> lack of preload decreases perfusion and causes syncope
#6651

142
Q

What is Crowe sign?

A

The most specific sign of NF-1

-> axillary freckling

143
Q

A patient presents with 5 days of increased urination, muscle cramps, pain, and weakness. Current medications include simvastatin and furosemide. What is the most likely diagnosis?

A

Hypokalemia -> check electrolytes first.

Hypokalemia can cause muscle cramps, fatigue, muscle spasm, and weakness

Rhabdomyolysis due to statin use presents more acutely with blood in the urine.

144
Q

Where does copper deposit in the eye in Wilson disease?

A

Descemet membrane of the CORNEA

145
Q

What is dysplastic nevus syndrome?

A 
A syndrome where dysplastic nevi (compound nevi with atypical mitoses which may be precursors to melanoma) are formed due to loss of a CDK4 inhibitor (tumor suppressor) on chromosome 9
#6674
146
Q

What marker definitively differentiates between partial and complete hydatidiform mole?

A

p57 - paternally imprinted and thus only maternally expressed
-> if maternal tissue is present, it is a partial mole

147
Q

Both Salmonella and Pseudomonas are lactose non-fermenters. How do you differentiate between them based on lab tests?

A

Salmonella - oxidase negative, also makes H2S

Pseudomonas - oxidase positive

148
Q

What rash can be associated with reactive arthritis?

A

Formation of vesicles which become sterile pustules and keratotic scaling -> keratoderma blenorrhagica

Ulcers on the penis can also be seen

149
Q

What is the most common liver neoplasm of children and its tumor marker?

A

Hepatoblastoma - alpha-fetoprotein

150
Q

Will the patient tilt their head towards or away from the affected eye in a CN4 palsy? Will diplopia be worse going up or downstairs?

A

Turn their head away, so affected eye will be held in extorsion (loss of intorsion), and unaffected eye will intort to keep plane of vision parallel

Diplopia is worse going downstairs since SO functions to depress the eye in adduction (also bad when looking down when reading).

151
Q

Why might a VSD not be detectable at birth?

A 
Takes about a week for pulmonary vascular resistance to fully drop -> left to right shunting becomes loud enough to hear
#203
152
Q

What is CD10 a marker of in ALL?

A

Pre-B cells. I just put this in cuz you might trip up and think its T cells cuz it’s a low number

153
Q

What protein do Aflatoxins cause a mutation of?

A

P53 protein - increased risk of HCC

154
Q

What does ST elevation in leads V1/V2 probably indicate?

A

Proximal LAD STEMI

155
Q

What condition is marked by agenesis of the cerebellar vermis?

A

Dandy-Walker syndrome

-> also causes enlargement of 4th ventricle, and is associated with noncommunicating (obstructive) hydrocephalus

156
Q

What early glycolysis enzyme in the liver is upregulated by insulin?

A

Glucokinase u fuckboy!!

157
Q

What is the calculation for oxygen content of blood?

A

(1.34 * Hb * SaO2) + (0.003 x PaO2)

1st half of equation is oxygen bound to Hb:

Hb = 15 g/dL average
1.34 mL O2/gram Hb
SaO2 is the hemoglobin saturation %

2nd half of the equation is the oxygen dissolved in plasma alone:

0.003 mL O2 / mmHg O2

158
Q

What is the Oxygen delivery to tissues equal to?

A

Oxygen content of blood (mL O2 / dL of blood) * Cardiac output

159
Q

What is diffusion rate of a gas equal to?

A

Diffusion coefficient of gas (intrinsic) * Area * (P1-P2) * (1/Thickness)

Diffusion of gas decreases with a loss of area (i.e. emphysema)

Diffusion of gas decreases with a gain in thickness (i.e. pulmonary fibrosis)

P1-P2 is the difference in partial pressures

160
Q

What is the alveolar gas equation?

A

PAO2 = PIO2 - PaCO2 / R

R = VCO2 / VO2 -> usually 0.8

PIO2 = (760-47)*0.21 = 150 mmHg usually

161
Q

What form of hemoglobin does CO2 prefer to bind? What effect is this called?

A

The deoxygenated (Taut) form of hemoglobin

  • > explains why CO2 is released at the lungs, and why carbaminohemoglobin compounds are most important in venous blood
  • > this is called the “Haldane effect”
162
Q

Will Cl- content be higher in arterial or venous blood?

A

Arterial blood

Venous “chloride shift” occurs when CO2 is buffered in RBC to HCO3-, and is exchanged with Cl- at the membrane
-> Cl- enters RBC, reducing venous Cl- concentration

163
Q

What is the Bohr effect?

A

Release of H+ from the tissue promotes oxygen release from hemoglobin at the tissue level

164
Q

What are average ICF / ECF volumes relative to body weight?

A

60-40-20 rule

60% = total body water
40% = ICF
20% = ECF
165
Q

What’s the equation for filtration fraction?

A

FF = GFR/RPF

Normal = 20%

166
Q

How will increasing the plasma protein concentration affect GFR / RPF?

A

Increasing colloid osmotic pressure of plasma -> decrease force for filtration into urine -> decrease GFR

RPF is relatively unchanged, thus FF will decrease

167
Q

What is the FeNa?

A

Fractional excretion of sodium

FeNa = Na+ excreted / Na+ filtered

Na+ excreted = U*V -> urine concentration of Na+ times urine flow rate

Na+ filtered = GFR * plasma concentration of sodium (filtered load)

168
Q

What is meant by renal “threshold” and what is it for glucose?

A

The plasma concentration at which the urinary excretion is no longer 0 (Tm mechanisms begin to be exceeded)

169
Q

What is the approximate Tm for glucose? What is Tm?

A

Tm = 375 mg/min, average ability of a tubule to reabsorb glucose (attempting to compensate for GFR * plasma concentration, aka the filtered load)
-> remember that Tm is the sum of all transporters abilities in a tubule

170
Q

For a patient with a plasma glucose of 1,000 mg/dL, what is their true plasma [Na] after correction if their current [Na] is 120 mg/dL?

A

For every 100 mg/dL above 200 mg/dL, the plasma [Na] will go up 1.6 mM

(1,000-200)/100 = 8
8*1.6 = 12.8
12.8 + 120 = 132.8 mmol/L

Thus, this patient’s Na would still be low, and the patient would have excess TBW.

171
Q

Give the Henderson Hasselbach Equation.

A

pH = 6.1 + log (([HCO3-]) / (0.03 *pCO2))

The 0.03 is based on dissolved carbonic acid

172
Q

What condition is more associated with hypomagnesemia, Bartter or Gitelman Syndrome?

A

Gitelman syndrome, despite it being a NCC defect. Cuz fuck logic lolololololololo!!!!!

173
Q

What condition presents like primary hyperaldosteronism, but aldosterone is undetectable? Treatment?

A

Liddle syndrome - Gain of Function mutation in ENaC

Treatment: Amiloride

174
Q

What is the treatment for syndrome of apparent mineralocorticoid excess?

A

Exogenous corticosteroids, which cannot activate the mineralocortoid receptor and thus do not require 11B-hydroxysteroid DH

175
Q

What are two ways in which angiotensin II works in the brain?

A
  1. Hypothalamus - directly stimulates thirst

2. Stimulates ADH release via posterior pituitary

176
Q

What cells release erythropoietin from the kidney?

A

Interstitial cells of the peritubular capillary bed within the cortex
-> in response to hypoxia

177
Q

What cells does ADH act on in the collecting duct?

A

Principle cells - (same ones with ENaC / ROMK) -> where AQP2 is upregualted

Inner medullary collecting duct cells - Urea resorption to increase the gradient

178
Q

Why does hypocalcemia prolong the QT interval?

A

Ca+2 influx is needed to inactivate the L-type Ca+2 channels

-> conditions of hypocalcemia will make it take longer for enough calcium to rush in, thus prolonging the QT

179
Q

What electrolyte disturbances can hypomagnesemia cause and how?

A

Hypokalemia - Mg+2 needed to inhibit ROMK

Hypocalcemia - Mg+2 needed to inhibit CaSR -> tetany

180
Q

How does hypomagnesemia cause Torsades?

A

Hypokalemia -> induces TdP (along with U waves)
Hypocalcemia -> prolonges the QT

Hypo-Mg also induces TdP alone by an unknown mechanism (but is used to treat the condition)

181
Q

What EKG disturbances are seen in hyperkalemia?

A

Wide QRS and peaked T waves

182
Q

What are the symptoms of hypermagnesemia?

A

Physiologic calcium blocker -> decreased Deep Tendon Reflexes, bradycardia, cardiac arrest (due to heart block)
-> Ca+2 influx needed for pacemakers

183
Q

What two electrolyte imbalances can cause nephrogenic DI?

A

Hypercalcemia -> exacerbates Na/Ca loss together -> hypovolemia

Hypokalemia

184
Q

How do you calculate compensation of metabolic acidosis? How do you calculate anion gap?

A

Winters formula:
PaCO2 = 1.5(HCO3-) + 8 +/-2

Anion gap:
Na - (HCO3- + Cl-)

185
Q

What is the definition of increased anion gap and what are the causes of increased anion gap metabolic acidosis?

A

Increased: Anion gap >12 mEq/L

MUDPILES
M: Methanol, metformin
U: Uremia
D: Diabetic ketoacidosis / starvation ketoacidosis 
P: Paracetamol - acetaminophen
I: Isoniazid, Iron tablets
L: Lactic acidosis
E: Ethylene glycol
S: Salicylates
186
Q

What is dilutional hyperchloremic acidosis? Where does this appear in the mnemonic for normal anion gap metabolic acidosis?

A

Rapid ECF expansion via NaCl will dilute out the current concentration of HCO3-, making the body relatively acidic

HARDASS
Hyperalimentation - high HCl levels in food
Addison disease - Type IV RTA 
Renal tubular acidosis
Diarrhea - HCO3- / K+ loss
Acetazolamide - Type II RTA
Spironolactone - Type IV RTA
Saline infusion - Dilutional
187
Q

What is the most common site of obstruction in kidney development, which can be detect as hydronephrosis on prenatal ultrasound?

A

Ureteropelvic junction (UPJ) -> last to canalize

This is the junction between the ureter and the renal pelvis

188
Q

Why are ACE inhibitors / ARBs teratogenic?

A

AT2 is required for normal renal development

-> will cause oligohydramnios -> Potter sequence if taken in utero

189
Q

What does water under the bridge mean for males vs females?

A

Males - vas deferens goes above the ureter

Females - uterine artery goes above ureter

190
Q

What autosomal disorder is marked by progressive tubulointerstitial fibrosis and progressive renal insufficiency, with inability to concentrate urine? How will kidneys appear on ultrasound?

A

Medullary cystic kidney disease

Kidneys appear shrunken / fibrosed on ultrasound

191
Q

What are the periods of lung development up until age 20? What develops in each of these stages?

A

Lung bud = 4-6 weeks - up to segmental bronchi
Pseudoglandular period = 6-16 weeks - up to terminal bronchioles
Canalicular period = 16-26 weeks - up to alveolar ducts
Saccular / Alveolar period = 26 weeks to term - up to terminal sacs
Alveolar period = birth to 10 years - up to adult alveoli number

10-20 years - HYPERTROPHY of existing alveoli

192
Q

What hernia is associated with resultant pulmonary hypoplasia? Where does it occur?

A

Congenital diaphragmatic hernia

-> usually left-sided

193
Q

Where do Type II pneumocytes release their surfactant from?

A

Lamellar bodies (dark bodies in cytoplasm)

194
Q

What do the left and right horns of sinus venosus become?

A

Remember than sinus venosus is the structure that drains the veins into the atria

Left - Coronary sinus

Right - Smooth part of right atrium (sinus venarum)

195
Q

How is foramen ovale formed? How is the valve formed?

A

When septum secundum grows to the edge of the perforated septum primum (foramen secundum), but does not quite reach the endocardial cushions. The remaining portion of the septum primum becomes the valve of foramen ovale.

-> Foramen ovale is the space between septum secundum and foramen secundum (the hole in septum primum)

196
Q

What fails to fuse to cause patent foramen ovale?

A

Failure of septum primum (valve of foramen ovale) and septum secundum to fuse
-> can cause paradoxical emboli

197
Q

What cofactor is necessary for dopamine beta hydroxylase? What does this enzyme do?

A

Vitamin C

Converts Dopamine to norepinephrine

198
Q

How does vitamin E affect the INR?

A

Increases the INR

-> vitamin E is a competitive inhibitor of gamma-carboxylation

199
Q

What is the rate-limiting step of the TCA cycle and what downregulates it?

A

Isocitrate dehydrogenase

-> downregulated by ATP, NADH

200
Q

What enzyme of the glycogen processing pathway does cortisol affect?

A

Upregulates glycogen synthase, as does Glucose-6-phosphate and insulin
-> wants to store sugar in times of stress

201
Q

What cation is responsible for upregulation of Pyruvate dehydrogenase, isocitrate dehydrogenase, and a-KG dehydrogenase?

A

Calcium! Makes sense because when your muscles are contracting you want more ATP!

202
Q

What poisoning is characterized by vomiting, rice-water stools, garlic breath, and QT prolongation?

A

Arsenic! Inhibition of lipoic acid and circumventing of glycolysis enzymes so it neds 0 ATP
-> lipoic acid seen in PDH and aKG dehydrogenase

203
Q

How is PDH deficiency inherited and what are its clinical symptoms? How is it treated?

A

X-linked
Neurologic defects, with lactic acidosis and increased serum alanine starting in infancy
Treatment: Ketogenic diet, with increased lysine and leucine (purely ketogenic)

204
Q

Tell me how the following agents inhibit the ETC:

  1. Rotenone
  2. Antimycin A
  3. Oligomycin
  4. Aspirin overdose
A
  1. Rotenone - inhibition of complex 1
  2. Antimycin A - inhibition of complex 3. “Ant-3-mycin”
  3. Oligomycin - remember the Fo subunit of ATP synthase -> inhibits ATP synthase (o=oligomycin sensitivity)
  4. Aspirin overdose - uncoupling agent, like 2,4-DNP
205
Q

Where is glucose-6-phosphatase present?

A

The endoplasmic reticulum! G6P is actually shipped into the ER for cleavage and release as glucose!

206
Q

What are the nonessential amino acids?

A

These are ones which you can synthesize from a carbon skeleton

Alanine (ALT)
Serine
Glycine (-MeTHF from serine)
Proline (from glutamate)
Glutamate (from aKG)
Glutamine (+NH3)
Aspartate (from oxaloacetate)
Asparagine (+NH3)
*Cysteine (depends on Methionine as sulfur donor to serine)
*Tyrosine (depends on phenylalanine precursor)
207
Q

What are the purely glucogenic essential amino acids?

A

I “met his val”entine and she is so “sweet”

methionine
histidine
valine

208
Q

In what ways to tryptophan and arginine utilize tetrahydrobiopterin (BH4)?

A

Tryptophan -> serotonin required BH4 + B6.

Arginine -> nitric oxide requires BH4

209
Q

How is creatine made?

A

Glycine + Arginine combine in a multistep pathway

210
Q

Why is pencillamine a treatment option for cystinuria?

A

Bbinds with cysteine to yield a mixed disulfide which is more soluble than cystine

211
Q

What is the mechanism by which all pathways converge to increase glycogenolysis during muscle contraction and epinephrine + glucagon (liver only) hitting the cell?

A

Beta receptors + glucagon -> activate PKA, which phosphorylates glycogen phosphorylase kinase (GPK)

Calcium + alpha receptors -> increase calcium -> calcium-calmodulin increases glycogen phosphorylase kinase

Glycogen phosphorylase kinase phosphorylates glycogen phosphorylase
-> activates it

Remember that insulin will dephosphorylate all these processes -> decrease glycogenolysis

212
Q

How do you distinguish Cori disease from Von Gierke disease?

A

Cori disease - lactate will be normal, and muscles will also be involved (hypotonia). Limit dextrans in cytoplasm.

von Gierke - high lactate levels (G6P pushed to lactate), and only liver involved.

213
Q

What enzyme is deficient in Hunter syndrome and what accumulates in urine?

A

Iduronate sulfatase -> need to take sulfate groups off uronic acid sugars before they can be cleaved by alpha-iduronidase

Same accumulation as Hurler: heparan and dermatan sulfate

Think “HD”

214
Q

What are the clinical features of Hunter syndrome which distinguish it from Hurler?

A

Hunter has no corneal clouding

  • > onset generally slightly later and milder as well, with AGGRESSIVE behavior -> Hunters are aggressive
  • > both still have deafness, stiff joints, coarse facial features, etc
215
Q

What enzyme is deficient in Metachromatic leukodystrophy and what will accumulate?

A

Arylsulfatase A - galactocerebroside sulfate will accumulate in Schwann cells / oligodendrocytes (a major component of myelin membranes)

216
Q

How is Krabbe disease diagnosed / what are the symptoms?

A

Central and peripheral neuropathy (demyelinating, like metachromatic leukodystrophy). Especially optic atrophy.

-> makes sense because galactocerebrosides are the substrates on which sulfatides are made.

**Globoid cells -> macrophages in globoid shape from lipid accumulation

Galactocerebroside and psychosine accumulate

217
Q

What are the late symptoms of Fabry disease?

A
  1. Progressive renal failure (podocytes accumulate Gb3, leading to proteinuria)
  2. Cardiovascular disease
  3. Cerebrovascular disease (strokes)
    - > vascular damage.
218
Q

How many calories are in one gram of alcohol?

A

Number of letters in the word:

1g alcohol = 7 kcal

carb = 4 kcal
fatty acid = 9 kcal

219
Q

What is the function of CETP? Why might blockage be useful?

A

Cholesterol Ester Transfer Protein - Functions to transfer cholesterol esters from HDL to VLDL / IDL / chylomicron remnants

-> blockage could ultimately stop the formation of LDL particles, which get concentrated with cholesterol from HDL transfer via CETP

220
Q

What is the function of LCAT? What is needed to active it?

A

LCAT = Lecithin cholesterol acyltransferase
Esterifies plasma cholesterol released from tissues so they can be uptaken by HDL (so they will be hydrophobic enough)

Needs Lipoprotein A-1 to activate it.
A1 = Activates

Apo-A1 is considered the principle protein in HDL

221
Q

What is Type III hyperlipoproteinemia and what is the inheritance pattern? Mechanism?

A

Dysbetalipoproteinemia - rare autosomal recessive condition of ApoE defect

  • > Chylomicrons, VLDL, and IDL do not properly bind the LDL receptor (Apo B/E receptor)
  • > Increased blood levels of these remnants increases triglycerides and total cholesterol

REMEMBER it’s dysBETAlipoproteinemia because lipids of the B-48 and B-100 lineages are abnormal (defective ApoE). LDL is okay because there is no ApoE, and where does HDL even come from lol.

222
Q

What is Type I dyslipidemia also called and what are the two causes? Inheritance pattern?

A

Hyperchylomicronemia - autosomal recessive

Increased chylomicrons, and triglyceride levels due to either:
1. Lipoprotein lipase deficiency
or
2. Apolipoprotein C-II deficiency (co-factor for LPL)

223
Q

What are the clinical findings of hyperchylomicronemia? Is there an increased risk of atherosclerosis?

A
  1. Pancreatitis -> due to high triglycerides
  2. Hepatosplenomegaly
  3. Eruptive xanthomas - papules on buttocks and back due to triglyceride accumulates
  4. Lipemia retinalis - capillaries in back of eye look white
224
Q

What is Type IV dyslipidemia called and what causes it? Inheritance pattern? Symptoms?

A

Hypertriglyceridemia -> autosomal DOMINANT due to overproduction of VLDL

High TGs with risk of pancreatitis if TGs > 1000 mg/dL

Eruptive xanthomas -> similar reasoning as hyperchylomicronemia

225
Q

What causes abetalipoproteinemia? What are the symptoms?

A

Deficiency in Apo B48 (Chylo) and ApoB100 (VLDL and others) -> severe fat malabsorption and failure to thrive
-> basically the opposite of dysbetalipoproteinemia where these lines cannot be taken up due to ApoE effect

  • > vitamin E deficiency
  • > spinocerebellar degeneration, retinitis pigmentosa, progressive ataxia
  • > acanthocytosis
  • > restrict fats from diet, use large doses of vitamin E
226
Q

Give the arteries travelled around one trip of the circle of Willis, starting at basilar artery

A

Top of basilar artery -> P1 segment of PCA -> PCA junction -> posterior communicating artery -> MCA/ICA junction -> A1 segment of ACA -> anterior communicating artery -> A1 segment of ACA -> MCA/ICA junction -> posterior communicating artery -> PCA junction -> P1 segment of PCA -> top of basilar artery.

227
Q

What is the only CN without a thalamic relay to the cortex?

A

CN1 - olfaction

-> primary cortex is piriform cortex in medial temporal lobe

228
Q

What is the function of the dorsal motor nucleus of X vs nucleus ambiguus of X?

A

Dorsal motor nucleus - sends autonomic parasympathetic fibers to heart, lungs, and GI tract

Nucleus ambiguus - motor innervation of swallowing only -> i.e. gag / cough reflex efferents

229
Q

Which is the only muscle of mastication involved in both protrusion and active opening of the mouth?

A

Lateral pterygoid

-> think “lateral lowers”

230
Q

What’s the number 1 way to tell apart lenticulostriate artery stroke from entire middle cerebral artery stroke?

A

There will be contralateral paralysis and/or sensory loss, but absent cortical signs (i.e. neglect, aphasia, visual field defect)

231
Q

Are the anterior or posterior spinal arteries paired?

A

Posterior!

Anterior there is only one, since there is only one anterior median fissure in the spinal cord.

232
Q

What causes inferior alternating hemiplegia? Symptoms?

A

Infarct of proximal branches of anterior spinal artery as it comes off of vertebral artery, or vertebral artery branches

-> loss of blood supply to mid medulla level -> 10-12 M and M’s, remember

Inferior alternating hemiplegia = contralateral UMN signs + CN12 palsy (ipsilateral tongue deviation) -> also called medial medullary syndrome

Loss of medial lemniscus -> decreased contralateral proprioception as well (internal arcuate fibers already crossed)

233
Q

What is Wallenberg’s syndrome also known as and what causes it?

A

Lateral Medullary Syndrome - caused by destruction of PICA, which damages all structures around dorsolateral mid-medulla levels, including inferior cerebellar peduncle

Remember this one is the “don’t PICA hoarse that can’t eat”

234
Q

What are the symptoms of lateral medullary syndrome?

A

ALS damage -> contralateral
Nucleus ambiguus damage -> dysphagia, hoarse voice, uvula deviation to contralateral side, decreased gag reflex
Spinal nucleus / tract of V -> ipsilateral pain / temp on face
Inferior cerebllar penduncle -> posterior spinocerebellar tract / CCT loss = ataxia from lack of unconscious proprioception
Horner’s syndrome -> loss of descending reticulospinal fibers which activate sympathetics, ipsilateral ptosis, miosis, anhydrosis

235
Q

What causes lower lateral pontine syndrome? Where does this artery go?

A

Destruction or occlusion of AICA, this artery wraps around CN 7 / 8 at the cerebellopontine angle, also supplies middle cerebellar peduncle

236
Q

What are the symptoms of lower lateral pontine syndrome?

A

“Facial droop, AICA’s pooped”

facial paralysis, dry eye (facial nerve is PANS to lacrimal gland), decreased salivation (loss of sublingual / submandibular), loss of taste on anterior 2/3, deafness (CN8), nystagmus to opposite side (no input from ipsilateral side, fast reset the other way)

Signs similar to PICA - Horner syndrome may also occur, as well as loss of contralateral ALS and ipsilateral spinal nucleus of V

237
Q

What structures is an Anterior communicating artery vs Posterior communicating artery aneurysm most likely to compress?

A

AComm - Compression of optic chiasm -> bitemporal hemianopsia

PComm - Compression of ipsilateral CN3 -> Ipsilateral CN3 palsy

238
Q

What disease is accumulation of ubiquitinated TDP-43 associated with?

A

Frontotemporal dementia or Amylotrophic Lateral Sclerosis

Remember that Pick’s disease is mainly a tau-opathy

239
Q

What are pick bodies?

A

Inclusions of hyperphosphorylated Tau protein

Seen in:
Pick’s disease (Frontotemporal dementia)
Alzheimer’s
Progressive Supranuclear Palsy

240
Q

What is the CSF finding in AIDP & why was this important?

A

Albuminocytologic dissociation -> elevated CSF protein with normal WBC count. Important because it differentiated from polio which had similar clinical findings but is associated with increased WBCs as well.

-> increased protein thought to reflect the widespread inflammation of the nerve roots

241
Q

What is acute disseminated encephalomyelitis, who tends to get it, and what causes it? (This is new to you).

A

Disease of multifocal inflammation and demyelination in the CNS

Usually occurs in children post infection or rarely vaccination.

Distinguish from MS by lack of relapses and also extreme severity -> can cause coma / altered mental status

242
Q

What condition is associated with cerebellar hemangioblastomas?

A

Von Hippel Lindau

-> just remember it is also associated with RCCs and Pheochromocytomas since it helps wipe out hypoxia-inducible factor

243
Q

What are the clinical manifestations of NF-2?

A

Think of “2”
2 eyes = bilateral cataracts
2 ears = bilateral acoustic schwannomas (Verocay bodies / myxoid regions are Antoni A / B)
2 brains = meningiomas and ependymomas (ependymal cells line the ventricles and spinal cords)

244
Q

What is the function of the artery of Adamkiewicz and what happens if it’s knocked out?

A

Supplies the anterior spinal artery below T8
If knocked out: anterior cord syndrome:
Loss of UMN below lesion
Loss of LMN at level of lesion
Loss of ALS system
Dorsal columns spared (posterior spinal supply)

245
Q

What is Cauda equina vs Conus Medullaris Syndrome?

A

Conus Medullaris - injury of UMN within spinal cord down to L2 (level of conus medullaris) -> presents as areflexic / dysfunctional bladder due to loss of UMN inhibition

Cauda Equina - Injury to LMN below L2, due to tumor / compression -> saddle anesthesia, absent reflexes, radicular pain

246
Q

How do facial nerve UMN lesions differentially affect the face?

A

Forehead - spared, due to bilateral innervation

Lower face - receive only contralateral innervation, will be completely lost

247
Q

What is Ramsay Hunt syndrome?

A

Reactivation of herpes zoster in the geniculate ganglion

  • > ipsilateral facial paralysis (Bell’s palsy)
  • > ear pain -> geniculate ganglion is the sensory for part of the ear
  • > vesicles on face / ear
248
Q

Are high frequency sounds processed best at the base or the apex of the cochlea?

A

High frequency - base (near origin)

Low frequency - apex (near helicotrema)

249
Q

Which drainage pathway do muscarinic agonists vs prostaglandin agonists affect?

A

Muscarinic agonists - trabecular outflow -> via trabecular meshwork / Canal of Schlemm

Prostaglandins - uveoscleral outflow -> drainage into uvea (vascular layer made of iris, ciliary body, and choroid layer) + sclera (continuous with cornea)

250
Q

Will blockage of the trabecular meshwork cause open-angle gluacoma or closed-angle glaucoma?

A

Open-angle! Can be blocked by uveitis (WBCs), vitreous hemorrhage (RBCs), or retinal elements (retinal detachment)

-> think of open angle as analogous to communicating hydrocephalus, but of the eye

251
Q

What is the cause of closed-angle glaucoma?

A

Analogous to noncommunicating hydrocephalus
-> obstruction of normal aqueous humor flow through pupil (posterior chamber) -> fluid builds in posterior chamber and compresses iris to obstruct / close the angle which allows aqeous humor to flow through trabecular meshwork

252
Q

Where do deposits accumulate in dry ARMD?

A

Between Bruch’s membrane (of choroid layer, outermost) and retinal pigment epithelium

Drusen deposits -> gradual loss of central vision (vs glaucoma = peripheral vision)

253
Q

Where do vessels proliferate in wet ARMD?

A

choroid layer -> responsible for supplying blood to outer 1/3 of retina
-> neovascularization can be stopped via ranibizumab or bevacizumab

254
Q

What is the cause of retinitis pigmentosa and what generally occurs first?

A

Inherited disease of retinal degeneration

-> rods are generally affected first, so night blindness precedes total vsual loss

255
Q

Does the superior oblique muscle intort or depress the eye in adduction?

A

Depresses the eye in adduction

Think a”D”duction = “D”epression

Also just remember that the angle is more natural when the eye is in abduction -> inferior rectus would more naturally depress the eye at this angle

256
Q

In what gaze will a superior oblique palsy be most noticeable?

A

Looking away from affected side, the eye will shoot upward (loss of depression in adduction)

Step 1 Miscellanous (40 decks)

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