U-World (advanced editing) Flashcards
Guy has chest trauma from motor vehicle accident. Breath sounds are normal bilaterally. Has elevated JVP and a drop in BP by 15 mmHg on inspiration. What does he have?
Cardiac tamponade (presents with Beck triad: hypotension, distended neck veins/ elevated JVP, and distant heart sounds).
He has Pulsus Paradoxus from the cardiac tamponade, which means a drop in BP of greater than 10mmHg on inspiration (it is normal for there to be a slight drop in BP on inspiration bc more blood is coming into the right heart, so the RV pushes into the LV and the LV has a little less space/ blood to pump out. But normally, the left heart wall is strong and pushes back. In cardiac tamponade it is not, so there’s a bigger bulge and a greater drop in BP).
College-aged girl. Swollen lymph nodes and palpable spleen. Histo pic looks like this. What is the diagnosis? What is shown in this histo pic?
Infectious mononucleosis (from EBV, rarely CMV)
Reactive lymphocytes (cytotoxic T-cells)- note they are large, scalloped, and have abundant cytoplasm (vs normal lymphocytes that are small, round, and have minimal cytoplasm)
What are these WBCs? What do they release?
Reactive lymphocytes= cytotoxic T-cells and NKCs that are pathogen-specific (specific to intracellular infections like HIV, CMV, toxoplasmosis, diagnostic for mono…). They are large, scalloped, and have abundant cytoplasm (vs normal lymphocytes that are small, round, and have minimal cytoplasm). They have cytotoxic granules—> release perforin (punch holes in infected cell’s membrane) and granzymes (enter cytoplasm of infected cells and trigger cell death), released in response to MHC I of host cells expressing foreign antigen.
What is the initial cellular event triggered by Digoxin? Explain its mechanism of action and 2 net effects.
It initially decreases sodium efflux (leaving) myocardial cells.
MECHANISM: blocks Na+/K+ pump so that Na+ can’t go out and K+ can’t come in—> more Na+ in the cell—> since there’s more Na+ in the cell, Na+ won’t come in through Na+/Ca2+ exchanger—> less Ca2+ leaving means more Ca2+ stays in the myocyte to help with contraction. SO, Digoxin increases contractility. It also stimulates the vagus nerve to decrease HR.
Mechanism of SSRI’s?
(SSRI= selective serotonin reuptake inhibitor)
Block the serotonin transporters (on the pre-synaptic cleft to prevent re-uptake and thus increase serotonin in the synaptic cleft)
(*note: SSRIs do NOT block serotonin receptors on the post-synaptic side)
Patient is anxious and takes a bunch of medication. She now is found with flushed skin, dry oral mucosa, and dilated pupils not responding normally to light. She overdosed on what medication?
TCA’s (tricyclic antidepressants) (Imipramine, Amitriptyline, Nortiptyline)
Remember, TCAs have anti-muscurinic effects
Name the 5 receptors TCA (tricyclic antidepressants) act on and the consequences (side effects).
Note that TCAs work as antidepressants because they block NE and serotonin reuptake—> inc NE and serotonin available in the synaptic cleft. The fact that TCAs also affect these other 4 receptors is bad—means they come with a big side effect profile.
How does Botox work to relax muscles?
Botulinum toxin cleaves SNARE proteins so that they cannot cause docking of neurotransmitter vesicles—> neurotransmitter (ACh) release to relay the signal in the NMJ for the muscle to contract
What is going on with this guy?
Internuclear ophthalmoplagia (INO)
A disorder of horizontal gaze. The MLF (in dorsal pons) is damaged—> impaired communication between CN 3 and 6. In this case, the left dorsal pons has a problem—> impaired adduction of ipsilateral eyes (the guy can’t look in with his left eye)
What is this?
Oral Herpes (HSV-1)
”dew drops on a rose pedal”
Herpes virus stays latent in the dorsal root ganglia of nerves. What transport protein carries it back there? What transport protein carries it back up to reactivate in stress?
Dynein= moves things backward (carries Herpes virus backward to be latent in dorsal root ganglia)
Kinesin= moves things forward (carries Herpes virus frontward to the skin to reactivate)
mnemonic: Dynein sounds like dinosaurs, which go way back in time (carries things back). Kinesin sounds like kinetic energy, which is energy moving things forward.
What is the genetic cause of fragile X syndrome? What are some features you see in a fragile X patient?
Increased CGG repeats on X chromosome—> hypermethylation and inactivation of FMR1 gene.
intellectual disability, prominent chin, large testes
(remember CGG repeats and protruding Chin + Giant Gonads)
Label B
middle cerebral artery (MCA)
Label D
Posterior cerebral artery (PCA)
Label A
Anterior cerebral artery (ACA)
Label E
Basilar artery
Label the little arteries coming off of “H”
Lenticulostriate arteries
Name the biggest orange structure.
Thalamus
Name the top 2 white structures.
Lateral ventricles.
Name the little orange structures up top.
Caudate nucleus
Name the thing on that’s being pointed to at the bottom of the brain cross section.
hippocampus
What nerve is responsible for:
- taste + sensation to posterior (back) 1/3rd of tongue?
- taste to anterior (front) 2/3rds of tongue?
- sensation to anterior (front) 2/3rds of tongue?
- taste + sensation to posterior (back) 1/3rd of tongue? CN 9 (glossopharyngeal)
- taste to anterior (front) 2/3rds of tongue? CN 7 (specifically the chorda typani, a branch off the facial nerve)
- sensation to anterior (front) 2/3rds of tongue? CN 5 (specifically the lingual nerve, a branch off V3, or the mandibular nerve, part of the trigeminal nerve)
What hormone shares the same precursor as opioids?
ACTH—> cortisol (coming from CRH—> POMC pathway that also gives rise to beta-endorphins which are opioids)
*note that this relationship suggests stress and opioid pathways have a strong relationship
Explain why/ how sickling of RBCs occurs in sickle cell anemia. Be sure to explain how stress can bring on a vaso-occlusive crisis.
Sickled cells have a Glu (hydrophilic)—> Val (hydrophobic) mutation so part of the RBC hates water and wants to get away from it—> sickles inward. This isn’t too much of an issue until stress comes along and disturbs pH (for example, think of exercise which causes acidosis—> inc H+). This makes the RBC with the mutation freak out bc it’s trying to get away from that charge and it’s suddenly surrounded by more charge so it sickles inward even more and these sickles cells stack on top of each other and occlude vessels—> vaso-occlusive crisis, pain, problems!
Mom had no prenatal care. Baby is born with jaundice, hepatomegaly, edema, low hemoglobin, nucleated erythrocytes, respiratory distress, and pleural effusions. Baby dies. What did baby have?
Hemolytic disease of the newborn
Rh negative mom had 2nd baby who was Rh positive
So her body made antibodies against the 1st Rh positive baby during birthing when her blood mixed with baby’s. So 2nd baby’s RBCs got attacked by those antibodies and destroyed. Jaundice, hepatomegaly are due to destruction of RBCs—> more bilirubin breakdown product. There’s more nucleated (immature erythrocytes) bc bone marrow is trying to compensate for RBC destruction by making more RBCs. Inadequate blood results in serious complications and death.
What receptor is mutated in hemochromatosis?
There is an HFE gene mutation in the transferrin receptor.
Since the transferrin receptor is defected (and it’s job is to detect iron levels in the blood), it thinks there’s no Fe in the blood even though there are actually high levels. So it won’t trigger release of hepcidin from liver hepatocytes like it normally does, so hepcidin won’t be there to inhibit Ferroprotin channels on enterocytes—> more Fe will be absorped into blood, worsening the problem. In simple terms, hemocromotosis= Iron overload. The classic triad of symptoms is cirrhosis, DM, and skin pigmentation (“bronze diabetes”).
Which coagulation factors are involved in the intrinsic pathway? Extrinsic pathway? Common pathway (shared by both)?
Intrinsic—> 12, 11, 9, 8
extrinsic—> 7
common—> 10, 5, 2, 1
“Loss of expression mutation for gene coding for a protein on hepatocytes and enterocytes that interacts with transferrin receptor.” <—This confusing explanation describes what disease?
Hemochromatosis!
Since the transferrin receptor is defected (and it’s job is to detect iron levels in the blood), it thinks there’s no Fe in the blood even though there are actually high levels. So it won’t trigger release of hepcidin from liver hepatocytes like it normally does, so hepcidin won’t be there to inhibit Ferroprotin channels on enterocytes—> more Fe will be absorped into blood, worsening the problem. In simple terms, hemocromotosis= Iron overload. The classic triad of symptoms is cirrhosis, DM, and skin pigmentation (“bronze diabetes”).
PTT corresponds to what part of the coagulation cascade? PT corresponds to what part?
PTT—> intrinsic pathway (coagulation factors 12, 11, 9, 8)
PT—> extrinsic pathway (coagulation factor 7)
Protein C and S inhibit what coagulation factors?
5 and 7
Vitamin K activates what coagulation factors? Thrombin activates what coagulation factors? Where do Warfarin and Heparin act to cause anti-coagulation?
Based on this histo picture alone, what’s the cancer diagnosis?
AML (you see Auer rods, then it is acute myeloid leukemia)
Why are fractures, bone pain, and hypercalcemia often seen in multiple myeloma?
Malignancy of plasma cells—> release cytokines and OSTEOCLAST ACTIVATING FACTORS that directly stimulate the RANK receptors on osteoclasts—> more bone breakdown, bone pain, and hypercalcemia (calcium released from bone)
In multiple myeloma, light chains can deposit in the kidney, leading to proteinuria and renal failure. They can also deposit in tissues leading to what??
Amyloidosis
How can multiple myeloma cause proteinuria?
Malignancy of plasma cells—> too much IgG light chains produced—> light chains deposit into kidney tubules and clog them up—> renal failure and you pee out these “Bence Jones proteins”—> proteinuria Malignancy of plasma cells—> too much IgG light chains produced—> light chains deposit into kidney tubules and clog them up—> renal failure and you pee out these “Bence Jones proteins”—> proteinuria
What are rouleaux formations and why are they seen in multiple myeloma?
Stuck together RBC formations
Seen in MM because it’s a malignancy of plasma cells—> too much IgG (especially light chains) gets produced, so there’s high serum protein (from the Ig’s) and this makes RBCs stick together like glue
What spike is seen in multiple myeloma?
M spike (indicative of lots of immunoglobulin, which in the case of MM it is IgG)
Why do Multiple Myeloma patients have an increased risk for infection?
Malignant plasma cells—> making too much IgG, not enough antigenic variation (normally different kinds of antibodies are produced to handle different kinds of infections)—> increased risk for infection!!
*infection is the #1 cause of death in MM patients
Name the types of non-Hodgkin lymphoma.
- 3 small cell types
- 1 medium cell type
- 1 large cell type
Small-cell non-Hodgkin lymphomas:
- Follicular lymphoma
- Mantle cell lymphoma
- Marginal cell lymphoma
Medium-cell non-Hodgkin lymphoma:
- Burkitt lymphoma
Large-cell non-Hodgkin lymphoma:
- Diffuse large B-cell lymphoma
The 3 types of small-cell non-Hodgkin lymphomas are:
- Follicular lymphoma
- Mantle cell lymphoma
- Marginal zone lyphoma
Name the translocation and gene that corresponds to each (except marginal zone we don’t need to know the gene).
- Follicular lymphoma—> t (14,18). Bcl2 (this is a regulator of apoptosis. So overexpresson of this—> apoptosis can’t be inhibited.)
- Mantle cell lymphoma—> t (11,14). Cyclin D1 (this is an oncogene, specifically a cell cycle regulator from G1–>S phase. So overexpression of this—> unregulated progression into S phase/ DNA synthesis of cell cycle.)
- Marginal zone lyphoma—> t (11,18).
Burkitt lymphoma is a medium-cell non-Hodgkin lymphoma. What virus is it associated with? What’s the translocation? What’s the gene? What pattern is seen on histo? What is the common patient demographic and presentation?
Burkitt lymphoma is associated with EBV (mono).
Translocation is t (8,14).
Gene is c-myc (an oncogene, specifically a nuclear/ transcription regulator, so overexpression of this—> too much transcription).
On histo, you see a starry sky appearance.
Most common in African boys and they present with enlarged jaw/ mandible (can also occur in abdomen in other kinds of people, but that’s a less commonly tested subset.)
What tumor marker for AML? ALL?
AML—> MPO+ (precipitates as “auer rod” granules)
ALL—> tDT+
Philadelphia chromosome t(9, 22) means what type of cancer? There are 2 options, but one is more common to have this translocation.
t (9,22) means it’s CML (chronic myeloid leukemia) or B-ALL (B-cell acute lymphoid leukemia) (the more severe version vs. t(12,21)). More than likely it will be CML.
Tear drop cells are seen in what myeloproliferative disorder and why?
Myelofibrosis
Too many megakaryocytes—> make lots of platelet-derived growth-factor (PDGF)—> bone marrow fibrosis—> the few RBCs made in the bone marrow get squished into “teardrops” as they try to exit.
What is a myeloproliferative disorder? What are the 4 types to know?
Myeloproliferative disorder= mutation up at the level of the hematopoietic stem cell leads to TOO MANY MATURE MYELOID CELLS.
- CML (chronic myeloid leukemia)- too many grnaulocytes, specifically basophils. *This is called chronic leukemia, but is technically a myeloproliferative disodrer.
- Polycythemia Vera (PV)- too many RBCs
- Essential thrombocythemia (ET)- too many platelets
- Myelofibrosis- too many megakaryocytes
**note: besides CML, all these involve JAK 2 Kinase mutations.
What is acute leukemia? What are the types to know?
Acute leukemia= too many Blasts (immature precursor blood cells)—> crowd out the bone marrow and interrupt normal hematopoesis (problems arise with this cancer bc dec mature RBCs—> anemia, dec mature neutrophils—> neutropenia, dec mature platelets—> thrombocytopenia and bleeding).
- *1. AML (Acute Myeloid Leukemia). Subtypes: APL (acute promyelocytic leukemia), acute monocytic leukemia, and acute megakaryoblastic leukemia.
2. ALL (Acute Lymphoblastic Leukemia). Subtypes: B-ALL and T-ALL.
What is chronic leukemia? What are the 4 types to know?
Chronic leukemia= too many mature lymphocytes.
- CLL (Chronic Lymphocytic Leukemia)- too many naive B-cells
- Hairy Cell Leukemia- too many mature B-cells
- ATLL (Adult T-cell Leukemia/ Lymphoma)- too many mature CD4+ t-cells
- MF (Mycosis Fungoides)- too many mature CD4+ t-cells *NOT a fungus!
What 2 blood conditions cause hyperviscous blood?
- Polycythemia Vera (myeloproliferative disorder where you have too many RBCs)
- Waldenstrom Macroglobulinemia (malignancy of plasma cells that results in overproduction of IgM, the big antibody—since it’s so big it binds to RBCs and causes them to aggregate)
Name the biochemical signaling pathway that is mutated in the following myeloproliferative disorders:
- PV (Polycythemia Vera), ET (Essential Thrombocythemia), and Myelofibrosis
- CML (Chronic Myeloid Leukemia)
- PV (Polycythemia Vera), ET (Essential Thrombocythemia), and Myelofibrosis—> JAK 2 Kinase
- CML (Chronic Myeloid Leukemia)—> Tyrosine kinase (*remember the tire swing. Also remember that CML is due to a t(9,22) translocation of BCR-ABL gene which causes more tyrosine kinase cell signaling)
These cells would stain positive for what?
MAO+
Notice the auer rods in these myeloid Blastic cells! This is AML (acute myeloblastic leukemia), probably the subtype APL (acute promylocytic leukemia) bc it is most know for its auer rods. Remember that auer rods are just MAO crystals preceipitating. It’s just a histological feature seen in this cancer type.
What is this cancer?
Multiple myeloma
Label A, B, C, D, E, F.
A- Pituitary gland
B- Thalamus
C- Pineal gland
D- Pons
E- Cerebellum
F- Medulla
What is the velocity equation we can use to describe speed of conduction across an axon? How does myelination and demyelination alter this equation?
Surgeons are planning to do a radiofrequency ablation on a patient to destroy the ectopic focus and treat the patient’s SVT arrhythmia at the crystal terminals of the Right Atrium. What nerve is close to this and at risk for getting damaged in the procedure?
The right Phrenic nerve
Stroke of what vessel would cause this (hemianopia with macular sparing)?
PCA (posterior cerebral artery)
*macular sparing occurs bc the macula has dual blood supply from the PCA + MCA. So even though the PCA is stroked out, the MCA is still supplying it with blood.
What is Myasthenia Gravis (MG)?
autoimmune disease where you have antibodies attacking ACh receptors at post-synaptic neurons—> weakness of muscles
What kind of arthritis?
Rheumatoid (osteoarthritis usually isn’t so prominent with fingers all messed up)
*this is called “ulnar deviation of the digits”
What do T-tubules do?
Allow for coordinated contractions of myofibrils in muscle fibers (T-tubules= spaces for action potentials to travel down so that all muscle fibers can contract together.)
A girl falls on her outstretched arm (hyperextension injury). As a result, she gets a supracondylar humeral fracture. What nerve is most likely to be injured?
radial nerve
What is thoracic outlet syndrome?
Compression of the nerves (lower trunk of brachial plexus)/ vessels as they leave the thorax through the scalene triangle (exit through the hole bordered by scalene muscles). This can result from scalene muscle hypertrophy, a mass in that region (like a lipoma or Pancoast tumor), or an extra rib (cervical rib) taking up space and narrowing the exit hole (as shown in this picture).
A boy is a pitcher for his baseball team. He presents with numbness in his right shoulder, arm, and fingers. He is mostly having numbness in his little finger. His medical history is unremarkable except that he has an extra rib. Diagnosis?
Thoracic outlet syndrome.
The extra cervical rib makes the space between the scalene muscles smaller for the nerves (lower brachial plexus) to exit out of. He is specifically getting compression to his ulnar nerve from it’s root—> numbness of pinky finger (remember the 1 1/2 fingers on pinky side= territory of ulnar nerve). *don’t get thrown off by the fact he is a pitcher and assume rotator cuff injury! This doesn’t affect nerves.
What step in the sliding filament model of muscle contraction involves ATP?
Myosin head DEtachment from actin.
Which region contains only thick, no thin, filament?
Thin= actin. Thick= myosin…So it’s asking what region contains only myosin, no actin.
That would be region E.
Lighter= actin. Darker= myosin. Not D because that is actin. Not B because that is myosin, however contains a region of crossover. E is just myosin like it’s asking.
Name the muscles and their nerve innervations.
A: Deltoid. Axillary nerve. (ABduction of arm to 15 degrees).
B: Infraspinatus. Suprascapular nerve. (Externally rotates the arm).
C: Latissimus Dorsi. Thoracodorsal nerve. (Extension, addiction, and medial rotation of the humerus).
D: Trapezius. CN 11 aka spinal accessory nerve. (Elevates, rotates, and stabilizes the scapula).
E: Triceps. Radial nerve. (Elbow extension).
This is the right knee. What’s the thin bone? What’s the thicker bone? Label A-F.
Thin bone= fibula (pinky toe side)
Thick bone= tibia
A- lateral meniscus (on lateral/ fibula/ pinky toe side)
B- LCL
C- ACL
D- PCL
E- medial meniscus (on medial/ tibia side)
What major hip flexor muscle is used when doing a sit up?
iliopsoas (psoas major + psoas minor + ilacus)
(connects to vertebrae on back and wraps to hip, so makes sense how it would support the back and allow you to sit up w/o using your hands)
If you have severe pain when you sit on your knees from bursitis (inflammation of bursae), what bursa is affected?
prepatellar bursa
You do the empty can test and patient is in pain. This means what is most likely injured? Be specific.
Rotator cuff injury, specifically impingement and most commonly in the supraspinatus.
Impingement from the tendon being sandwiched between the head of the humerus and the acromion during aBduction.
**supraspinatous tendionpathy is the #1 cause of rotator cuff injury.
What artery runs alongside the radial nerve?
The deep brachial artery.
We treat Parkinson’s with L-DOPA and also give with DOPA decarboxylase inhibitors (carbidopa) and sometimes also catechol-O-methyltransferase inhibitors (entacapone). Why do we give these drugs?
L-DOPA is given rather than dopamine directly bc dopamine cannot cross the BBB, L-DOPA (its precursor) can.
Carbidopa and Entacapone are often also given to reduce peripheral L-DOPA degradation/ metabolism (prevent L-DOPA from being broken down so that more gets to the brain and exerts its effect to help symptoms).
Patient recently had an abdominal/ pelvic surgery (for example, an appendectomy) and now presents with loss of sensation to the suprapubic area. What nerve was affected?
Iliohypogastric (T12-L1)
What nerve innervates muscles that do hip flexion/ knee extension and provides sensation to most of the leg in front?
femoral nerve
What nerve provides sensation to the upper medial thigh and innervates muscles that do adduction of the thighs?
Obturator nerve
Why can’t you prescribe a patient on SSRIs for depression Triptans for their migraines?
Due to risk of serotonin syndrome!
SSRIs block re-uptake of serotonin into pre-synaptic neuron—> more serotonin in the cleft.
Triptans are serotonin AGONISTS and stimulate serotonin receptors on the post-synaptic vessels—> increased effect of serotonin—> vasodilation.
If you increase serotonin in the cleft and increase the effect it has, serotonin syndrome may result and that is life-threatening.
How do triptans work for migraine abortion?
They are serotonin agonists, activate the serotonin receptors on the post-synaptic blood vessels—> vasoconstriction (**we think migraines are a result of vasodilation/ too much blood filling up in the brain area, so vasoconstriction helps- we now also think it’s not the vasoconstriction that helps directly, but other mechanistic things that result from vasoconstriction.)
*They also inhibit release of vasoactive peptides and molecules involved in pain.
