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Block 9 > U-World: Other > Flashcards

U-World: Other Flashcards

1
Q

Vaginal pH of 4-4.5 and less than a teaspoon of thick white vaginal discharge comes out daily. Diagnosis?

A

This is normal!

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2
Q

Painful menstrual periods and UNIFORMLY enlarged uterus. Diagnosis?

A

Adenomyosis (endometriosis in the myometrium)

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3
Q

Gravida 3, para 3. What does this mean?

A

3 pregnancies. 3 births.

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4
Q

Most common cause of mitral valve stenosis (accounts for 99% of cases)

A

Rheumatic heart disease

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5
Q

Thickening of mitral valve and diastolic murmur. What valvular problem? Most likely diagnosis?

A

Mitral valve stenosis (trouble opening the valve due to thickening from Aschoff bodies made of granulomas and giant cells from the bug)
Rheumatic heart dz

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6
Q

What 3 murmurs increase in intensity with the handgrip exercise?

A

(Handgrip= increasing afterload/ pressure the heart has to pump against)
1. Mitral regurgitation
2. Aortic regurgitation
3. VSD
(You are making it harder for blood to pump forward, so blood will take path of least resistance/ back flow. More blood through defective valve= increased murmur intensity.)

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7
Q

VSD (ventricular septal defect) is best heard where on cardiac auscultation?

A

Lower left sternal border/ tricuspid area

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8
Q

BNP is released in response to what?

A

Ventricular wall stretching

Remember, it does the opposite of the RAAS- acts in response to volume overload to lower volume/ BP

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9
Q

AIDS patient has confusion, ataxia, and motor problems. MRI of brain shows multifocal areas of white matter demyelinated (no mass effect or enhancement). Diagnosis?

A

JC virus

-can reactivate in HIV and can cause Progressive Multifocal Leukencephalopathy (PML). Slow progression of demyelination (remember wood peeling off the legs of the table in Sketchy)—> confusion, ataxia, and motor problems.

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10
Q

Which 2 blood vessels are most susceptible to atherosclerosis?

A

Lower abdominal aorta and coronary arteries.
Also, in general, arteries with bends/ branch points are more susceptible to atherosclerosis because they encourage turbulent blood flow.

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11
Q

Polyarteritis nodosa is a ________-vessel vasculitis that spares the ________.

A

MEDIUM-vessel vasculitis
Spares the LUNGS
(The inflammation affects renal arteries as well as arteries in other places like the heart, liver, GI tract, and even skin as palpable purpura, but spares the pulmonary arteries.)

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12
Q

Most common cause of acute pericarditis?

A

Viral infection (from adenovirus, coxsackievirus, echovirus, influenza virus, etc.)

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13
Q

Guy developed sharp chest pain 4 days ago. The pain gets worse on inspiration, gets better when he sits up and leads forward. Diagnosis?

A

Acute pericarditis (most likely due to a viral infection like coxsackievirus)

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14
Q

Systolic murmur in a young person heard best at the left lower sternal border. Decreases in intensity with handgrip. What is it?

A

HOCM (hypertrophic obstructive cardiomyopathy)
There’s an thickening/ out-pouching of the LV wall that makes it harder for blood to go out of aortic outflow tract. Handgrip= increase afterload that the heart has to pump against= makes it even harder for blood to get out from LV—> aorta= less blood going through defective valve= not as loud of a murmur.

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15
Q

Are the following measures increased/ decreased/ large/ small/ impaired/ normal in a patient with HOCM (hypertrophic obstructive cardiomyopathy)?

  1. LV Muscle mass
  2. LV cavity size
  3. Ejection fraction
  4. LV relaxation
A
  1. LV muscle mass is INCREASED (due to thickening of LV wall)
  2. LV cavity size is SMALL (thickened LV wall gets in the way of aortic outflow, so less space for blood in the LV compared to normal)
  3. EF is PRESERVED (contractility is not affected)
  4. LV relaxation is IMPAIRED (the hypertrophy impaired the LV’s ability to relax)
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16
Q

Systolic murmur heard best at left sternal border. Louder with Valsava maneuver. What is it?

A

HOCM (hypertrophic obstructive cardiomyopathy)
Valsava maneuver= bearing down (squeezing abdominal muscles, clamping the IVC)= decreasing preload= makes HOCM worse bc less blood to fill up the LV and push the problem (thickened LV wall obstructing outflow through aorta) out of the way= louder murmur.

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17
Q

Football player complains of SOB during hard training at practices. You hear a systolic murmur at his left sternal border. Diagnosis?

A

HOCM (hypertrophic obstructive cardiomyopathy)

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18
Q

How can a beta-blocker help a patient with HOCM (hypertrophic obstructive cardiomyopathy)?

A

Beta-blocker—> decreases HR and contractility—> gives the heart more time to fill with blood in diastole before pumping again. This improves symptoms bc more preload pushes the defect (hypertrophied LV wall obstructing aortic outflow) out of the way and makes the problem better!

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19
Q

The anti-fungal agent amphotericin B (amp B) binds to what to excrete its anti-fungal effects?

A

Binds to ergosterol (the cholesterol equivalent on fungal cells—> forms holes in fungal cell membrane). *note: while it targets ergosterol, it binds cholesterol to some degree (on normal body cells), which is why it has nasty side effects.

(Sketchy pharm: “non-sterol” sign and holes in frog tank in science lab class)

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20
Q

What do the prefixes “-epi” and “-sub” mean?

A

Epi means above (think of epi sounding like epinephrine/ adrenaline which you get when you skydive ABOVE land in the sky)
Sub means below (think of a submarine BELOW the water)

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21
Q

Why might you have an elevated Creatine in multiple myeloma?

A

Multiple myeloma= malignancy of plasma cells—> overproduction of antibodies (light chains)—> get filtered through kidney and cause damage to kidney

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22
Q

How can multiple myeloma cause bone fracture and hypercalcemia?

A

Malignant plasma cells release cytokines—> activate osteoClasts (more bone breakdown)—> lyric lesions (“punched out” bone)—> inc serum calcium= hypercalcemia

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23
Q

Where are fractures most likely to happen in multiple myeloma?

A

The vertebrae

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24
Q

What bone lesions are produced by prostate cancer metastasis to the vertebrae? What bone lesions are produced by multiple myeloma (fractures often also in the vertebrae)?

A

Prostate cancer mets to vertebrae—> osteoBlastic lesions (add to the bone)—> radiopaque (more white, you can see it on X-ray)

Multiple myeloma fractures to vertebrae—> osteolytic lesions—> radiolucent (more see-through, can’t see it well on X-ray)

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25
Q

What does radiopaque mean? Radiolucent?

A

Radiopaque—> CAN see it on X-ray (more whitish)

Radiolucent—> CANNOT see it well on X-ray (more see-through)

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26
Q

African boy with right mandible mass. What type of cancer should you think of?

A

Burkitt lymphoma (associated with EBV)

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27
Q

Burkitt Lymphoma is due to what translocation?

A

t(8,14)

The c-MYC oncogene on chromosome 8 gets translocated onto chromosome 14 (IgG heavy chain)—> overexpression of c-MYC—> too much transcription activation

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28
Q

C-myc, N-myc, L-myc are what type of genes?

A

Oncogenes- specifically, transcription activators/ nuclear regulators

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29
Q

HER 2 neu, RET, and Kit are what type of genes?

A

Oncogenes- specifically, growth factor receptors

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30
Q

RAS and ABL are what type of genes?

A

Oncogenes- specifically, signal transducers

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31
Q

Cyclin D1 and CDK 4 are what type of genes?

A

Oncogenes- specifically, cell cycle regulators

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32
Q

p53 and Rb are what type of genes?

A

Tumor suppressor genes

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33
Q

What do proto-oncogenes do? How many mutations to become an oncogene?

A

Cell growth and differentiation

1 mutation

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34
Q

What do tumor suppressor genes do? How many mutations are necessary for a tumor suppressor gene to turn into cancer?

A

Regulate cell growth (so they inhibit tumor formation)

2 mutations

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35
Q

What type of gene is Bcl2?

A

Regulator of apoptosis

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36
Q

Why do target cells form?

A

If erythrocytes have too much surface-to-area-volume ratio

(Note that target cells are usually associated with beta thalassemia and the bleb in the middle is due to decreased hemoglobin, but can be seen in other cases too…iron deficiency anemia where there’s reduced cell volume, obstructive liver disease, or after a splenectomy when there’s excessive membrane)

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37
Q

What is immune thrombocytopenia?

A

Antibodies against platelets

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38
Q

Why can target cells be seen after splenectomy?

A

The spleen removes excess membrane from RBCs. If you don’t have a spleen anymore, excess membrane will be present on target cells—> bleb in center= target cells (but eventually the liver takes over this role of the spleen and target cells are no longer seen)

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39
Q

Bloody diarrhea, high BUN and Cr, fragmented erythrocytes. What is it?

A

HUS (hemolytic uremic syndrome) caused by E. Coli 0157:H7

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40
Q

What is the triad of problems seen in HUS (hemolytic uremic syndrome)? Explain why each happens.

A
  1. Hemolytic anemia
  2. Thrombocytopenia (dec platelets)
  3. renal failure/ AKI

This usually results from EHEC (E.Coli 0157:H7) because the Shiga-like toxin damages endothelial cells in capillaries—> vWF on endothelial collagen is exposed and causes platelets to stick—> dec platelets available in the blood bc they are sticking in clumps—> hemolytic anemia bc RBCs get sheared into shistocytes as they go past the platelet clumps. Shiga toxin also damages the kidney.

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41
Q

What test do the lab people do to test for sickle cell anemia?

A

Hemoglobin electrophoresis (get a blood sample, centrifuge it down, and watch the Hb move on plate faster or slower…abnormal Hb moves slower than normal Hb)

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42
Q

Mom has no disease but had a kid with sickle cell anemia. Then she gets remarried. How can we know the chances their kid will get sickle cell?

A

Do a paternal hemoglobin electrophoresis (the test for sickle cell anemia- but just on the dad bc we already know mom is a carrier. She must be a carrier bc sickle cell is autosomal recessive and her kid with another husband had it so she’s a carrier)

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43
Q

What’s the mnemonic for remembering when to do southern/ northern/ western blots?

A

“SNoW DRoP”

Southern- DNA
Northern- RNA
Western- Protein

(SNoW= Southern/ Northern/ Western, DRoP= DNA/ RNA/ Protein)

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44
Q

ALL more likely in kids or adults?

A

Kids- more likely to have ALL

Exception: Down syndrome kids <5 years are more likely to have AML

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45
Q

AML more likely in kids or adults?

A

Adults- more likely to have AML

Exception: Down syndrome adults >5 years more likely to have ALL

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46
Q

You see a pedigree and only boys have the disease. What inheritance pattern can you pretty much assume it is?

A

X-linked (recessive or dominant)

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47
Q

What is a normal Hemoglobin? Normal Hematocrit?

A

Normal Hb= about 12-13 (specifically, 13.5-17.5 in guys and 12.5-17.5 in gals)

Normal Hematocrit= 3 times the normal Hb
(35-55% ish)

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48
Q

“Bleeding from venipuncture sites.” What’s the answer until proven otherwise?

A

DIC (disseminated Intravascular coagulation)

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49
Q

What is DIC (Disseminated Intravascular coagulation)?

A

Inappropriate activation of the coagulation cascade
(Coagulation factors and platelets are being used up where they shouldn’t be—> bleeding out from IV sites and mucosal surfaces)

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50
Q

Sickle cell anemia patient has a really low reticulocyte count. What does this mean?

A

The bone marrow is not responding appropriately to the anemia, so there’s a bone marrow problem (the bone marrow SHOULD be pumping out those erythrocytes/ RBC precursor cells like crazy to try to compensate for the low RBC levels)

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51
Q

What virus can cause aplastic crisis in a patient with Sickle Cell anemia?

A

Parvovirus B19 (non-enveloped, single-stranded DNA virus)

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52
Q

What amino acid change occurs in sickle cell anemia?

A

Glutamic acid (hydrophilic)—> valine (hydrophobic)

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53
Q

Explain “autosplenectomy” in sickle cell patients (why their spleens can get fibrotic and brown).

A

Vaso-occlusion to splenic vessels and the fact that the spleen is working in overdrive all the time to remove messed up RBCs—> the spleen pretty much dies off and becomes equivalent to someone w/o a spleen at all.

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54
Q

What is a direct Coomb’s test? Indirect Coomb’s test?

A

Direct Coomb’s—> patient has RBCs with antibodies on them and you put in antibodies (anti-IgG) and if it sticks to detect this it’s a positive test

Indirect Coomb’s—> patient has antibodies floating around in their blood and you put in RBCs with antibodies on them and if it sticks (agglutination) it’s a positive test

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55
Q

Patient is bleeding. PT and PTT are prolonged. Platelets and fibrinogen are low. Diagnosis?

A

DIC (Disseminated Intravascular coagulation)

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56
Q

“Lymphocytes with cytoplasmic projections” is describing what type of cancer?

A

Hairy cell leukemia

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57
Q

Hairy cell leukemia neoplasticism B cells (with cytoplasmic processes) are positive for what enzyme?

A

TRAP (tartrate-resistant acid phosphatase)

Memory trick: “things get TRAPped in hairy projections”

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58
Q

Guy has splenomegaly, pancytopenia, and bone marrow cannot be aspirated. Diagnosis?

A

Hairy cell leukemia

Note that “bone marrow cannot be aspirated” is termed “dry tap”

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59
Q

Pedigree shows females passing down a disease to all kids, but males are not passing it down. Inheritance pattern?

A

Mitochondrial

Kids get all their mitochondria from mom’s eggs—not from dad’s sperm

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60
Q

Give Rhogam to who?

A

A Rh negative mom pregnant with a Rh positive baby

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61
Q

Will EPO levels be increased, decreased, or normal in a patient with CKD (chronic kidney disease)? RCC (renal cell carcinoma)?

A

CKD—> decreased EPO (kidney is failing and kidney makes some EPO, so now you’ve got less of it given that the kidney is not doing its job)

RCC—> increased EPO (this is a cancer so you have MORE renal cells going crazy and pumping out the EPO)

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62
Q

Patient has hemolytic anemia, hypercoagulation, and pancytopenia. Deficiency in CD55 and CD59. Diagnosis?

A

Paroxysmal Nocturnal Hemoglobinuria (PNH)

PNH is a normocytic anemia. Mutation in PIGA gene—> defected GPI anchoring protein aka CD55 and defected DAF (decay accelerating factor)/ MIRL (membrane inhibitor of reactive lysis) aka CD59 (note that these all protect RBCs from their deadly neighbor…complement)—> complement destroys RBCs (hemolytic anemia).
Classic triad: hemolytic anemia (RBCs getting destroyed by complement), hypercoagulation (complement activates platelets), and pancytopenia (RBCs destroyed and WBCs + platelets getting used up so all low).
*you also see hemoglobinemia, hemoglobinuria (dark urine), and hemosidenuria in these patients.

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63
Q

What is pancytopenia?

A

Low platelets, WBCs, and RBCs (not an absence of- that would be aplastic anemia)

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64
Q

What is PNH (paroxysmal nocturnal hemoglobinuria)? State what the mutation is in, what there is a deficiency of, classic triad of symptoms, and other symptoms seen in these patients.

A

Normocytic anemia. Mutation in PIGA gene—> defected GPI anchoring protein aka CD55 and defected DAF (decay accelerating factor)/ MIRL (membrane inhibitor of reactive lysis) aka CD59 (note that these all protect RBCs from their deadly neighbor…complement)—> complement destroys RBCs (hemolytic anemia).
Classic triad: hemolytic anemia (RBCs getting destroyed by complement), hypercoagulation (complement activates platelets), and pancytopenia (RBCs destroyed and WBCs + platelets getting used up so all low).
*you also see hemoglobinemia, hemoglobinuria (dark urine), and hemosidenuria in these patients.

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65
Q

What type of breast cancer is most aggressive. How to treat?

A

HER 2 neu receptor positive breast cancer is more aggressive (compared to estrogen and progesterone positive types). Can treat with the monoclonal antibody Trastuzumab.

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66
Q

Kaposi sarcoma is due to what virus in HIV folks?

A

HHV 8 (human herpes virus 8)

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67
Q

A lady has CKD (chronic kidney disease). Now has a low reticulocyte count, normal iron levels. What is going on?

A

Anemia because CKD (failing kidneys)—> low EPO (kidneys not making EPO like they are supposed to)

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68
Q

A lady has CKD (chronic kidney disease). Now has a low reticulocyte count, normal iron levels. She is treated with a recombinant glycoprotein. In normal human language, what was she treated with?

A

EPO

CKD (failing kidneys)—> low EPO (kidneys failing to make EPO)—> anemia
Treat by giving EPO! STEP 1 likes to describe this as “recombinant glycoprotein.”

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69
Q

HOW does EPO lead to formation of more RBCs? (What kind of cell signaling does it use to cause this effect?)

A

JAK2/STAT signaling

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70
Q

No erythroid precursors, but everything else in blood labs checks out fine. What is this? What tumor is it associated with?

A

Pure red cell aplasia.

Thymic tumor

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71
Q

Thymic tumor is associated with what blood problem?

A

Pure red cell aplasia (no erythrocyte precursors)

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72
Q

You give a mom Rhogam because she is Rh negative pregnant with a Rh positive baby. What immunoglobulin class is it?

A

IgG

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73
Q

Cytokeratin is a marker for what cancer type/ lineage?

A

Epithelial cell carcinomas

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74
Q

Why is it important that babies get a vitamin K shot after birth?

A

Vitamin K activates coagulation factors (2, 7, 9, 10, protein C and S). Low vitamin K (due to poor placental transfer, low vitamin K content in breast milk, and baby’s liver that is still developing)—> coagulation factors aren’t getting activated to clot blood—> you get bleeding (and this can include bleeding into the brain!)

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75
Q

What 3 cytokines mediate cachexia?

A

TNF-alpha
IL-1
IL-6

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76
Q

Baby has a head in the 99th percentile and CT confirms Intravascular hemorrhage. Baby was born prematurely. What is probably the cause of the bleed?

A

Neonatal intraventricular hemorrhage (originating from the germinal matrix)

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77
Q

Baby has a head in the 99th percentile and CT confirms Intravascular hemorrhage. Baby was not vaccinated. What is probably the cause of the bleed?

A

Vitamin K deficiency (babies are normally always given a vitamin K vaccine after birth but mom refused it)—> decreased clotting (bc you need vitamin K to activate coagulation factors)

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78
Q

African American boy in a heme question. What should immediately come to mind?

A

Sickle cell anemia!

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79
Q

African American boy has swollen hands and feet and cries when you touch them. His brother died of a Strep pneumo infection. What does this boy have?

A

Sickle Cell anemia
(Note that he’s an African American boy, dactylitis (painful swelling of hands and feet) from vaso-occlusion, brother died of an encapsulated infection more likely in Sickle Cell patients suggesting there’s a history of it in the fam)

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80
Q

Are the following levels increased or decreased in a Sickle Cell Anemia patient? Bilirubin, LDH (lactate dehydrogenase), haptoglobin.

A

Bilirubin—> increased
LDH—> increased
Haptoglobin—> decreased

Remember that there’s extravascular hemolysis (spleen getting rid of sickled RBCs) and Intravascular hemolysis (sickled RBCs getting lysed) going on in sickle cell anemia. As RBCs break down, they release breakdown products (bilirubin, LDH) so those are increased in the blood. Haptoglobin is decreased bc it’s getting used up picking up Hb in circulation.

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81
Q

What is haptoglobin?

A

Molecule that goes around and picks up Hemoglobin that’s circulating in the bloodstream (from hemolysis of RBCs).

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82
Q

Caseating granulomas of TB have what surface marker?

A

CD14

83
Q

What’s the classic triad of symptoms seen in hemochromatosis? What cancer are these patients at increased risk for?

A
  1. Cirrhosis, 2. DM, 3. Skin pigmentation (“bronze diabetes”)

Hepatocellular carcinoma

84
Q

Most common primary malignant brain tumor in adults?

A

Glioblastoma multiforme (BGM)

85
Q

Adult presents with headache. Brain mass is discovered. Biopsy shows necrosis and vascular proliferation. Diagnosis?

A

Glioblastoma multiforme (GBM)

This is the most common type of malignant brain cancer in adults and is characterized by necrosis and proliferation of blood vessels. (Also is usually in the cerebral hemisphere, crosses corpus collosum “butterfly lesion,” and is GFAP positive)

86
Q

What is Factor V Leiden?

A

A thrombosis (clotting) disorder in which you have a mutated factor 5 coagulation factor. Normally proteins C and S inhibit factor 5 and 7. But this mutated factor 5 makes it so that proteins C and S cannot shut it down—> factor 5 coagulation factor stays active—> HYPERCOAGULATION.

87
Q

A lady is discovered to have a mutation in her factor 5 coagulation factor. She is at increased risk for developing what?

A

DVT and PE.

Why? Because factor 5 gets mutated in a way that prevents it from being inhibited by proteins C and S—> factor 5 remains active—> HYPERCOAGULATION—> more likely to clot too much

88
Q

What is PNH (paroxysmal nocturnal hemoglobinuria)? (State the gene the mutation is in, what’s deficient, the general problem, and presentation of patients who have this.)

A

PIG A gene mutation—> decreased GPI anchoring protein and CD55 + CD59 proteins that protect against complement on RBCs (RBCs have a deadly neighbor…and it’s complement)—> hemolysis (RBCs get destroyed by complement).
Classic triad:
(1) hemolytic anemia (hemoglobinemia- there’s inc Hb floating around in the blood since RBCs are getting broken up)—> hemoglobinuria (dark urine in morning). Patients can also get hemosiderosis (iron deposits in the kidneys—since there’s excess Hb floating in the blood, too much for haptoglobin to go pick up, and that Hb gets further broken down to heme—> Fe + protoporphyrin and Fe deposits in kidneys).
(2) pancytopenia (less RBCs bc getting destroyed, WBCs and platelets bc being used up)
(3) thrombosis at atypical sites (possibly due to release of pro-thrombic factors from lysed RBCs.

89
Q

How can PNH (paroxysmal nocturnal hemoglobinuria) cause hemosiderosis (iron deposits in the kidneys)?

A

It is a hemolytic anemia (complement destroys RBCs because they are lacking proteins that normally protect against complement). RBCs break down—> hemoglobin floats around in blood—> so much of it that it overwhelms haptoglobin so it can’t possibly go around and pick up all that Hb—> Hb breaks further into Fe + protoporphyrin and so that Fe accumulates and deposits into the kidneys.

90
Q

Most common brain tumor in kids?

A

Pilocytic astrocytoma (benign tumor of astrocytes in the cerebellum, cystic lesion w/ nodule, biopsy shows Rosenthal fibers which are hairlike processes)

91
Q

Hodgkin’s lymphoma is associated with what tumor markers…CD?? And CD??

A

CD 15+ and CD 30+

92
Q

All the myeloproliferative disorders (CML, PV, ET, and myelofibrosis—except CML) involve what biochemical signaling pathway mutation?

A

JAK 2 Kinase mutation

93
Q

Looking at Hemoglobin levels, how can you tell if a person is normal vs. sickle cell trait vs. sickle cell anemia?

A

Normal: 99% HbA (the normal Hb), 0% HbS (sickled), <1% HbF (fetal Hb)

Sickle trait: 50-60% HbA (normal Hb), 35-45% HbS (sickled), <2% HbF (fetal Hb)
(These percents can vary…Just remember that there’s Sickled Hb present, but more normal Hb than sickled.)

Sickle cell: 0% HbA (normal Hb), 85-90% HbS (sickled), 5-15% HbF (fetal Hb)
(Just remember that there’s more Sickled Hb than normal Hb.)

94
Q

Why are sickled cell anemia patients and those with sickle cell trait (carriers) protected against malaria?

A

They have more fetal Hb than normal individuals, which malaria cannot attack (malaria infects normal Hb, or HbA).

95
Q

Carbon tetrachloride (CCl4) is a toxic substance (used in dry cleaning industry) that is metabolized in the liver P450 system and can cause fatty change in the liver and necrosis. How does it cause these liver changes?

A

Free radical injury

Page 7 of Pathoma

96
Q

The Rb gene (retinoblastoma) regulates what checkpoint in the cell cycle?

A

G1–> S phase

It is a tumor suppressor gene

97
Q

58 year old post-menopausal woman with low Hb. Most likely cause?

A

Iron deficiency anemia due to colon cancer (she is old and no longer menstruating, so colon cancer is the most likely etiology)

98
Q

Do you have high or low ferritin and transferrin in iron deficiency anemia and why?

A 
Low ferritin (binds Fe in storage sites)- iron is low, so it will get depleted from storage sites 
High transferrin (binds Fe in the blood)- more transferrin molecules are available floating around in the blood to bind to Fe
99
Q

What’s the term for the anemia caused by HUS (hemolytic uremic syndrome)?

A

Microangiopathic hemolytic anemia

100
Q

The following structures are derivatives from what pharyngeal arch? Maxillary process (—> Maxilla, zygoMatic bone), Mandibular process (—> Meckel cartilage, Mandible), Malleus and incus, sphenoMandibular ligament.

A

1st pharyngeal arch (CN 5= trigeminal nerve)

101
Q

The following structures are derivatives from what pharyngeal arch? Muscles of Mastication, Masseter, lateral and Medial pterygoids, Mylohyoid, anterior belly of the digastric, tensor tympani, anterior 2/3rds of the tongue, tensor veli palantini.

A

1st pharyngeal arch (CN 5= trigeminal nerve)

102
Q

The following structures are derivatives from what pharyngeal arch? Reichert cartilage: Stapes, Styloid process, lesser horn of hyoid, Stylohyoid ligament.

A

2nd pharyngeal arch (CN 7= facial nerve)

103
Q

The following structures are derivatives from what pharyngeal arch? Muscles of facial expression, Stapedius, Stylohyoid, platySma, posterior belly of digastric.

A

2nd pharyngeal arch (CN 7= facial nerve)

104
Q

The following structures are derivatives from what pharyngeal arch? Stylopharyngeus and greater horn of the hyoid.

A

3rd pharyngeal arch (CN 9= glossopharyngeal)

105
Q

The following structures are derivatives from what 2 pharyngeal arches? Aryteoids, Cricoid, Corniculate, Cuneiform, Thyroid.

A

4th/ 6th pharyngeal arches

106
Q

What 2 factors contribute most to angiogenesis (formation of new blood vessels), allowing tumors to get blood supply?

A
  1. Vascular Endothelial Growth Factor (VEGF)
  2. Fibroblast Growth Factor (FGF)

*note: the cytokines IL-1 and INF-gamma INDIRECTLY promote angiogenesis by stimulating VEGF

107
Q

Elderly patient has a history of HTN and DM. She presents with memory issues, some kind of dementia. Later dies of an MI. Biopsy of the brain shows Congo red staining of the hippocampus, patchy red deposits that turn yellow-green in polarized light. What did she have?

A

Alzheimer’s Disease (AD)

Even though she has a history of arterial infarcations that make you think of vascular dementia, it is AD because AD is diffuse but mainly affects the HIPPOCAMPUS and they are describing A-BETA AMYLOID deposits in AD, not vascular dementia. In addition, you’d expect glial scar formation on autopsy if it were vascular dementia.

108
Q

The CSF of an HIV patient shows yeasts on India Ink staining. Diagnosis? Where is the most common primary site of this infection?

A

Cryptococcus Neoformins Meningitis

Primary site of infection= lungs (from there can spread through the blood and infect the CNS/ meninges)

109
Q

The neurotransmitter (NT) ACh is involved in sympathetic, parasympathetic, or both neurons?

A

Both.
All PNS neurons use ACh as a NT (so associate it more with the PNS).
But some sympathetic neurons also use it.

110
Q

A patient has blurry vision when reading only after taking the 1st generation anti-histamine drug Diphenhydramine for allergies. Why can this be a side effect?

A

1st generation anti-histamines (Diphenhydramine, Dimenhydrinate, Chlorpheniramine, and Doxylamine) have anti-muscarinic effects. This means they have effects against the PNS (and blocking the PNS is like causing sympathetic symptoms). Remember that accommodation (rounding up of the lens to zoom into close objects, constriction of pupils, and convergence/ moving eyes inward) is under PNS control. So if you block the PNS—> lack of accommodation—> blurry close-up vision.

111
Q

What’s the difference between these terms: anticholinergic and anti-muscarinic?

A

Nothing. They are synonyms.

112
Q

What happens in accommodation of the eyes. Is it under sympathetic or parasympathetic control?

A
  1. Rounding up of the lens (accommodation of the lens) (ciliary muscles contract, zonular fibers relax)
  2. Constriction of pupils (miosis)
  3. Convergence (eyes move medially/ inward)
    Under PNS control
113
Q

State what the PNS vs. sympathetic NS do to the (1) pupil (constriction vs. dilation) and (2) aqueous humor production/ IOP (intraocular pressure).

A

PNS—> pupil constriction (and accommodation to focus on close-up objects), less aqueous humor production (so dec IOP)

SNS—> pupil dilation (you have to let more light into your eyes to be focused on far away bears and run from them), more aqueous humor production (so inc IOP) (eyes need that extra fluid to focus in a fight/ flight situation)

114
Q

Why do you get more infections in multiple myeloma? (Note that infection is the #1 cause of death in these patients.)

A

Decreased production of normal immunoglobulins

(Malignancy of plasma cells—> too much IgG immunoglobulin, especially light chains—> not enough antigenic diversity among these Ig’s + the Ig’s getting made aren’t of as good of quality—> infection risk is higher/ harder to fight off)

115
Q

What do the pilli of Neisseria Meningitis do?

A

Attach and colonize nasopharyngeal epithelium (pilli is it’s major virulence factor and this is the first step of how the bacteria causes problems)

116
Q

A kid has a brain tumor. He is having severe headaches and is unable to look up. What kind of brain tumor is this?

A

Pinealoma (tumor of the pineal gland)

Presents with vertical gaze palsy (compression of the tectum, which is a structure at the top of the midbrain responsible for auditory and visual reflexes—> inability to look up).
*these patients can also get obstructive hydrocephalus (compression of cerebral aqueduct) and precocious puberty in males (hCG production). Similar to germ cell tumors (testicular seminoma).

117
Q

A patient with a DVT is given a medication that prolongs PT and PTT, but has no effect on TT (thrombin time). What class of medication is this: (a) COX-inhibitor, (b) direct factor 7a inhbitor, (c) direct factor 10a inhibitor, (d) direct thrombin inhibitor, or (e) unfractionated heparin. Say why the wrong answers are wrong too.

A

(C) direct factor 10a inhibitor (blocking factor 10= blocking part of the common pathway, so will effect PT and PTT).

You can answer the Q just based on knowing the coagulation cascade and what factors are under the intrinsic (8, 9, 11, 12), extrinsic (7), and common pathways (5, 2, 1). COX-inhibitor is aspirin, which is an anti-platelet med and it’s wrong bc that would have on effect on primary, not secondary, hemostasis (so no change in PT, PTT, TT). Direct factor 7a inhibitor blocks factor 7 in the extrinsic pathway, so would only cause prolonged PT. Direct thrombin inhibitor would cause prolonged TT (also prolonged PT and PTT). Unfractionated heparin would cause prolonged PTT and TT, not PT (even though it seems like it would…memorize that heparin is monitored by change in PTT levels).

118
Q

Guy gets crutches after breaking his leg. Now presents with upper extremity weakness and numbness. Decreased grip strength and absent triceps reflex. What nerve has probably been compressed by the crunches?

A

Radial nerve

This is “crutch palsy” aka “Saturday night palsy” (can get it from sleeping with arm over a chair). Due to compression of the axilla—> pressure on radial nerve. Presents with wrist drop (extensor muscles affected), dec grip strength, loss of sensation over posterior arm/ forearm and dorsal hand.

119
Q

What surrounds the…
Lateral ventricles?
3rd ventricle?
4th ventricle?

A

Lateral ventricles- surrounded by motor fibers
3rd ventricle- by thalamus
4th ventricle- by cerebellum

120
Q

Baby has a head in the 98th percentile. CT reveals dilation of lateral ventricles. She is having trouble feeding. What does she have?

A

Hydrocephalus (more specifically, non-communicating bc the CSF pathway must be BLOCKED off between the lateral ventricles and 3rd ventricle in order for CSF fluid to only dilate the lateral ventricles).

Muscle hypertonicity (motor neurons surround the lateral ventricles. Damaged motor fibers up in the brain—> UMN signs which is spasticity bc remember, “kids go crazy w/o adult supervision”)

121
Q

Intellectual disability, prominent mandible, large testes. Diagnosis?

A

Fragile X syndrome

Remember, this is a mutation in the FMR1 (Fragile Mental Retardation 1 gene) on the X-chromosome—> CGG trinucleotide repeats. Remember CGG for prominent Chin and Giant Gonads.

122
Q

When asked to look straight forward, patients eye turns inferior and laterally. What CN palsy is this?

A

CN 3 palsy

“DOWN and OUT”

123
Q

What eye muscles are innervated by CN 3 (Oculomotor), CN 4 (Trochlear), and CN 6 (Abducens)?

A

CN 4 (Trochlear)—> Superior Oblique

CN 6 (Abducens)—> Lateral Rectus

CN 3 (Oculomotor)—> all the rest (superior rectus, medial rectus, inferior rectus, and inferior oblique)

124
Q

Aneurysm of what artery can lead to CN 3 palsy?

A

Posterior communicating artery (PCA)

125
Q

Dilated pupil, droopy eyelid, eye faced “down and out,” and diagonal diplopia. What CN palsy is this?

A

CN 3 palsy

126
Q

Most common cause of bacterial meningitis in adults?

A

Strep Pneumo! Remember “MOPS”= most common cause of meningitis, otitis media, pneumonia, and sinusitis.

127
Q

Most common cause of bacterial meningitis in adults. Lancet-shaped gram positive cocci in pairs. What bacteria is it?

A

Strep Pneumo

128
Q

A patient has meningitis. CSF shows neutrophils with low glucose. Is this bacterial, viral, or fungal/ TB?

A

Bacterial (neutrophils fight bacteria + bacteria consume glucose)

129
Q

A patient has meningitis. CSF shows lymphocytes with normal glucose. Is this bacterial, viral, or fungal/ TB?

A

Viral (lymphocytes fight virus/ fungus + viruses do NOT consume glucose)

130
Q

A patient has meningitis. CSF shows lymphocytes with low glucose. Is this bacterial, viral, or fungal/ TB?

A

Fungal/ TB (mycobacterial) (lymphocytes fight fungi/ viruses + fungi/ TB consume glucose)

131
Q

How do you treat febrile seizure? Does cooling the patient down (with ice packs, etc.) help?

A 
Supportive care (can give Tylenol/ ibuprofen to help with the seizure/ lower prostaglandins)
NO. In fact, this can cause shivering—> more seizures.

*cool the patient down in a heat stroke! This is serious.

132
Q

What are the “watershed areas” of the brain (more susceptible to ischemia)?

A
  1. Pyramidal neurons of the cerebral cortex (layers 3, 5, 6)
  2. Pyramidal neurons of the hippocampus (this area is the most susceptible to ischemia)
  3. Purkinje layer of cerebellum
133
Q

Baclofen is used to treat what symptom of MS (Multiple Sclerosis)?

A

Spasticity

134
Q

The anti-cancer drugs Etoposide and Teniposide inhibit what as their mechanism?

A

Topoisomerase II

135
Q

The anti-cancer drugs Irinotecan and Topotecan inhibit what as their mechanism?

A

Topoisomerase I

136
Q

In simple terms, what is tumor lysis syndrome?

A

Large number of tumor cells destroyed in a short period (such as in a high-grade leukemia/ lymphoma when on chemotherapy)—> life-threatening electrolyte imbalances

(*prevent and treat dish hydration, Allopurinol, and Rasburicase)

137
Q

What is the mechanism of action of the oncology drug Rasburicase? What is it used for?

A

Converts uric acid to more soluble metabolites.
Prevents and treats Tumor Lysis Syndrome (large # of tumor cells destroyed at once, usually leukemia/ lymphoma patient on chemo—> life-threatening electrolyte imbalances)

138
Q

Which CN palsy will cause: horizontal diplopia, vertical diplopia, diagonal diplopia?

A

CN 3 palsy—> diagonal diplopia
CN 4 palsy—> vertical diplopia
CN 6 palsy—> horizontal diplopia

139
Q

What is the main problem in Huntington’s disease?

A

Loss of GABAergic neurons in the caudate nucleus of the basal ganglia—> chorea (rapid, involuntary contraction of muscle)

140
Q

45-year-old has become aggravated, aggressive, has jerky movements. Diagnosis?

A

Huntington disease (presents in age 20-50 and is characterized by involuntary jerky muscle contractions due to loss of GABAergic neurons in the caudate nucleus of the basal ganglia).

141
Q

Glucose-6-phosphate deficiency (a normocytic anemia) follows what inheritance pattern?

A

X-linked recessive

142
Q

Hereditary spherocytosis (a normocytic anemia) follows what inheritance pattern?

A

Autosomal dominant

143
Q

What is glucose-6-phosphate deficiency (the normocytic anemia)?

A 
RBCs are surrounded by oxidative stress (for example, H2O2). So, they use the molecule glutathione to protect themselves from oxidative damage. G6PD is an enzyme that helps regenerate glutathione to protect the RBCs.
G6PD deficiency (it has reduced half life)—> glutathione can’t be regenerated as well—> RBCs are less protected against oxidative stress...so, in the event of oxidative stress (infection, drugs, fava beans, etc.) RBCs get messed up (Hb precipitates into “Heinz bodies” and splenic macrophages take a bite out of them—> “bite cells”).
144
Q

Hemolytic anemia involving RBCs with dark inclusions. What is it?

A

G6PD deficiency.
Dark inclusions are referring to “Heinz bodies” (G6PD normally protects against oxidative stress. In this condition, RBCs are more vulnerable to oxidative stress—> RBCs get messed up and the Hb precipitates out into these Heinz bodies that the spleen then takes a bite out of—> “bite cells”).

145
Q

What’s the deal-io with G6PD deficient patients and anti malaria drugs?

A

Anti malaria drugs can cause oxidative stress in these folks—> hemolytic anemia (same with infection, some other drugs, and fava beans)

146
Q

What is the most common inherited coagulation disorder?

A

Von Willebrand disease (secondary hemostasis disorder where there’s no vWF—> unstable factor 8–> prolonged bleeding)

147
Q

How do you treat Von Willebrand disease? What is the drug’s mechanism of action?

A

(VWF disease= no vWF—> unstable factor 8–> prolonged bleeding)

Treat with DESMOPRESSIN (ADH analog)
Induces release of vWF from Weibel-Palade bodies in the endothelial cells

148
Q

Inheritance pattern of von Willebrand disease?

A

Autosomal dominant

149
Q

Desmopressin can be given to treat:
(1) Hemophilia A and von Willebrand disease
(2) Central DI and nocturnal enuresis (bed wetting)
State the mechanism of action that Desmopressin takes to help (1) and (2).

A

(1) Desmopressin treats Hemophilia A (factor 8 deficiency) and vWF disease (no vWF—> unstable factor 8) by promoting release of vWF from Weibel Palade bodies of endothelial cells to stop bleeding.
(2) Desmopressin treats central DI (not making ADH) and bedwetting bc it’s an ADH analog and it binds to V2 ADH receptors in renal tubular cells—> more aquaporin channels—> more retention of water (pee out less water).

150
Q

What does myoclonus mean?

A

Involuntary muscle jerking

151
Q

Most common tumor of the adrenal medulla in kids

A

Neuroblastoma

152
Q

Kid <4 years old has abdominal mass, catecholamine breakdown products in urine, non arrhythmic movements of eyes in different directions, and myoclonus (jerking movements). Diagnosis?

A

Neuroblastoma (most common adrenal medulla tumor in kids)

153
Q

Is Northern, Southern, or Western blot best to use to determine if a gene is being transcribed?

A

Remember transcription= DNA—> RNA.
Remember “SNoW DRoP” (Southern= DNA, Northern= RNA, Western= Protein)
This is RNA, so use a Northern blot!!

154
Q

What are telomerases and what happens to them in cancer?

A

RNA dependent DNA polymerase that adds DNA to ends of chromosomes to avoid loss of genetic material in every duplication.
In cancer, telomerases are dysregulated so that the cancer cells can keep dividing uncontrollably.

155
Q

A boy has a blood disorder involving bleeding into his joints. What is it? Inheritance pattern?

A

Hemophilia A (deficiency of coagulation factor 8). X-linked recessive.

156
Q

“Muscle fibers with blotchy red appearance.” What genetic disease group is this? Inheritance pattern?

A 
Mitochondrial myopathies (collection of rare diseases with CNS problems, weakness, confusion, lactic acidosis where muscle biopsy shows “ragged red fibers” due to mitochondria proliferating like crazy trying to compensate for mitochondria that are not working) 
MITOCHONDRIAL inheritance (mom passes to all kids, dad cannot pass it down)
157
Q

What does Hereroplasmy mean?

A

Some of the mitochondrial DNA is abnormal (mixed between normal and mutated)

*remember, mitochondrial inheritance pattern is where mom passes it down to all kids, dad cannot pass down. Why? You get all your mitochondria from mom. 
Homoplastic mom (all abnormal mtDNA)—> all kids get dz 
Heteroplastic mom (some abnormal mtDNA)—> variable
158
Q

What does uniparental disomy mean?

A

You get the both copies of the gene from the same parent

159
Q

What class of receptors are intracellular?

A

Steroid hormone receptors (cortisol, aldosterone, and progesterone)

160
Q

Methylation of a gene to turn it off is called what?

A

Imprinting (this happens whenever you inherit a gene that doesn’t get expressed)

161
Q

Myopathy, nervous system dysfunction, lactic acidosis, and red fibers on muscle biopsy is consistent with a group of disorders that have what inheritance pattern?

A 
Mitochondrial inheritance (mom passes down to all her kids bc kids get all mitochondrial DNA from mom, dads cannot pass it down) 
(Mitochondrial myopathies)
162
Q

What do releasing factors do in translation?

A

Recognize stop codons and terminate protein synthesis
(tRNA does not bind to stop codons, rather these releasing factors to so that the RNA can be let go of when the work of making protein from it is complete)

163
Q

What are the stop codons?

A

UAA, UGA, UAG

“You are annoying, you go away, you are gone”

164
Q

You see an image of crystals in the synovial fluid of a patient. You’re thinking gout or pseudo-gout…what is the shape difference that would help you diagnose which one?

A

Gout—> needle-shaped crystals

Pseudo-gout—> Rhomboid-shaped crystals

165
Q

What are gout crystals made of? What are pseudo-gout crystals made of?

A

Gout—> uric acid crystals

Pseudo-gout—> calcium pyrophosphate crystals

166
Q

Crystals in the synovial fluid that are negatively birefringent. What is it?

A

GOUT

Negatively birefringent= when aligned parallel they appear yellow, when aligned perpendicular they appear blue

167
Q

Kid has a rash. Mom has swelling of joint. Diagnosis?

A

Parvovirus B19–> causes “slap cheek” rash in kids, arthritis in adults (mimics rheumatoid arthritis but goes away)

168
Q

Young boy has to use his hands and climb up on his legs to stand up from the ground. He has a deficiency in a sarcolema-cytoskeleton linker protein. Diagnosis?

A

Muscular dystrophy (mutation in Dystrophin gene, which helps to anchor muscle fibers in skeletal and cardiac muscle).

169
Q

Duchenne and Becker (milder form) muscular dystrophy result from a mutation in what gene? What does that gene do? Why is Becker milder?

A

Dystrophin gene, which helps to anchor muscle fibers in skeletal and cardiac muscle. Duchenne results from frameshift mutation—>Deleted Dystrophin. Becker results from a non-frameshift mutation, so it’s not as severe (mutation, but not full-on deletion of the Dystrophin gene).

170
Q

Most common benign tumor of the bone?

A

Osteochondroma

171
Q

Mnemonic for remembering wrist bones?

A

“So Long To Pinky, Here Comes The Thumb.”

Start on thumb side lower level of bones—> move toward pinky and back over toward thumb with counting

172
Q

Rheumatoid arthritis (RA) can affect what part of the spinal cord?

A

Cervical spine

(**this is clinically important bc if you intubate a patient with RA, it could kill them. Why? The RA auto-antibodies affect joints and also cervical vertebrae—> weakened neck bones. So if you intubate them you could cause trauma to the neck bones and they could cave in and compress the cervical spinal cord. Just in general, cervical spine instability can compress the spinal cord so its a serious complication.)

173
Q

What is dermatomyositis?

A

Autoimmune disease in which antibodies attack proximal muscles—> proximal muscle weakness (for ex, may have trouble walking up stairs). You also get skin finding (inflammatory features): heliotrope rash (periorbital, looks like eyeshadow) and Gattron papules (plaques over joints and hands). This condition can occur on its own or as a paraneoplastic syndrome secondary to cancer (such as ovary, lung, or pancreatic carcinoma).

174
Q

Lady with ovarian cancer has trouble getting up the stairs because her muscles are so weak. Also has plaques over her hands and a periorbital rash. Diagnosis?

A

Dermatomyositis
Autoimmune disease in which antibodies attack proximal muscles—> proximal muscle weakness (for ex, may have trouble walking up stairs). You also get skin finding (inflammatory features): heliotrope rash (periorbital, looks like eyeshadow) and Gattron papules (plaques over joints and hands). This condition can occur on its own or as a paraneoplastic syndrome secondary to cancer (such as ovary, lung, or pancreatic carcinoma).

175
Q

Patient is really short (dwarfism) and has a bulging forehead. Diagnosis?

A

Achondroplasia (common cause of dwarfism where you have impaired cartilage proliferation in the growth plate from fibroblast growth factor receptor 3 (FGFR3) mutation)

176
Q

What is heparin induced thrombocytopenia?

A

A bad reaction to heparin where the heparin binds to PF4 (platelet factor 4) and then antibodies get made against that complex (hep-PF4) and these antibodies also attack platelets—> thrombocytopenia (low platelet count) and platelet aggregation (leading to thrombosis/ blood clots)

Heparin is an anti-coagulant (“blood thinner”) so should break up blood clots. If you just gave a patient heparin and now they are getting new blood clots, think of this (a bad reaction to it).

177
Q

You give a lady heparin. 5 days later she presents with DVT and low platelet count. Why? Explain.

A

Heparin-induced thrombocytopenia.

This is a bad reaction to heparin, where hep binds PF4 (platelet factor 4) and forms complexes. Antibodies get made to these hep-PF4 complexes and these antibodies also attack platelets—> thrombocytopenia (low platelet count) and more platelet aggregation (antibodies stick platelets together)—> thrombosis/ clotting.

**Heparin is an anti-coagulant. It should stop clotting, not cause clotting! So whenever a patient who just got heparin starts having more clotting, think of this.

178
Q

Asthma + wrist-drop + p-ANCA/ MPO. What vasculitis is this?

A

Eosinophilic granulomatosis with polyangitis (Church-Strauss)

179
Q

What maintains the resting potential of a neuron?

A

K+ efflux and some Na+ influx—> maintains resting potential of -70mV(opposite of what the Na+/K+ pump does, which is pump 3 Na+ out for every 2 Na+ in)

*note that the Na+/K+ pump depolarizes back to normal after depolarization is over, and it’s constantly working. But once the membrane potential is stabilized again, the leaky K+ channels allowing K+ to go out of the cell keep the resting potential close to -70 (and there are some channels that bring Na+ in)

180
Q

What is another name for the flexor retinaculum?

A

Transverse carpal ligament

181
Q

What nerve provides sensation to the lateral 3 1/2 fingers (thumb side)? What nerve provides sensation to the medial 1 1/2 fingers (pinky side)? What nerve provides sensation to the dorsum of the hand (whole back side)?

A

Lateral 3 1/2 fingers (thumb side)—> median nerve
Medial 1 1/2 fingers (pinky side)—> ulnar nerve
Dorsum of hand (whole back of hand)—> radial nerve

182
Q

Numbness and tingling in fingers when typing. Atrophy of thenar eminence. Diagnosis?

A

Carpal tunnel syndrome
(Flexor retinaculum is compressing the median nerve—> tingling and numbness in median nerve territory, of 3 1/2 fingers on lateral/ thumb side. Since a branch of the median nerve is the recurrent median nerve and this provides motor innervation to the thenar area/ thumb so you can oppose the thumb, it makes sense that this can lead to atrophy of this muscle.)

183
Q

Are paraspinal muscles slow or fast twitch?

A

Slow twitch. They have lots of myoglobin and mitochondria= inc oxygen. They don’t fatigue easily, but maintain our posture!

184
Q

What muscle(s) aBduct the arm to 15 degrees? From 15 to 90 degrees? Raise the arm all the way up?

A

Supraspinatus—> to 15 degrees
Deltoid—> from 15 to 90 degrees
Trapezius and serratus anterior—> raise arm (the trapezius rotates the scapula so you can raise your arm and the serratus anterior holds the scapula down/ prevents winging)

185
Q

Winging of the scapula is due to what nerve issue?

A

Cut long thoracic nerve which supplies the serratus anterior (muscle the holds the scapula down upon lifting of the arms)

186
Q

Most common rotator cuff injured muscle?

A

Supraspinatus

187
Q

Scaphoid bone fracture can lead to what vascular issue?

A

Avascular necrosis (the scaphoid bone located in the anatomical snuff box bordered by the extensor pollicus longus and extensor pollicus brevis gets retrograde blood flow to it and is therefore prone to avascular necrosis)

188
Q

Which filament is thick and which is thin of actin and myosin??

A 
Thin= actin (remember when you are active you are thin)
Thick= myosin
189
Q

What nerve innervates the latissimus dorsi muscle?

A

Thoracodorsal nerve.

190
Q

Main function of quadriceps muscles?

A

Extension at the knee.

191
Q

Where do the quadriceps muscle tendon insert?

A

Tibial tuberosity (on the knee)

192
Q

Osgood-Schaltters is a common cause of knee pain in young athletes due to repetitive strain where?

A

The tibial tuberosity (site where quad muscles come together to a tendon and insert)

193
Q

What 3 major muscles are used to sit up (without use of hands)?

A
  1. External abdominal obliques
  2. Rectus abdominals
  3. Hip flexors, especially the iliopsoas (psoas major, psoas minor, and ilacus)
194
Q

What is a bursae?

A

Fluid-filled synovial sac that reduces friction

195
Q

Winging of the scapula occurs due to damage of what nerve? This can be a complication of what common surgery?

A

Long thoracic nerve. Mastectomy with axillary lymph node removal (axillary lymph nodes run laterally along the same path as the long thoracic nerve).

196
Q

What lower extremity nerve runs through fibers of the psoas major muscle?

A

Femoral nerve

197
Q

What findings do you see in a patient with damage to their femoral nerve?

A

Weakness of quads, loss of patellar reflex, and loss of sensation over anterior and medial thigh + leg

198
Q

Cannot extend wrist (have wrist drop). What nerve is damaged?

A

Radial nerve

*Wrist flexion—> done by the median (and ulnar) nerves
Wrist extension—> done by the radial nerve

If the radial nerve is messed up, flexion wins over and your wrist remains flexed/ can’t extend.

199
Q

What nerve innervates most forearm and wrist extensor muscles?

A

Radial nerve

200
Q

You break your arm (humerus) up at the shoulder area. What nerve is most likely to be damaged?

A

Axillary

Remember: humerus fractures, proximally to distally, follow the “ARM” mnemonic meaning Axiallary—> Radial—> Median

201
Q

You break your arm (humerus) midshaft. What nerve is most likely to be damaged?

A

Radial

Remember: humerus fractures, proximally to distally, follow the “ARM” mnemonic meaning Axiallary—> Radial—> Median

202
Q

You break your arm (humerus) down closer to the elbow. What nerve is most likely to be damaged?

A

Median

Remember: humerus fractures, proximally to distally, follow the “ARM” mnemonic meaning Axiallary—> Radial—> Median

203
Q

Patient has flattening of the deltoid. What nerve was damaged? If he broke his arm, what part of the humerus was probably broken?

A 
Axillary nerve (innervates the deltoid muscle)
Proximal humerus (for example, an anterior dislocation of the humerus) up near the shoulder

(Remember: humerus fractures, proximally to distally, follow the “ARM” mnemonic meaning Axiallary—> Radial—> Median)

204
Q

What nerve innervates the deltoid and teres minor and provides sensation to the lateral aspect of the shoulder?

A

Axillary nerve

Block 9 (6 decks)

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