First Aid Pics I Flashcards
- esophagus
- rib
- trachea
- SVC
- Brachiocephalic artery
- Left common carotid
- Aorta
- Scapula
- Vertebral foramen
Differentiate direct vs. indirect ELISA
ELISA = enzyme-linked immunosorbent assay- detects presence of either specific antigen or specific antibody in a pt’s blood sample
- Direct ELISA = use test antibody to see if antigen is present, Ab directly coupled to color-generating enzyme
- Indirect ELISA: use either test antigen or ab, then secondary ab is coupled to color-generating enzyme to detect ab-ag complex
Spleen: what is contained in the red vs. white pulp?
Red pulp is peripherally and contains RBCs
- white pulp centrally containing T cells in the periarteriolar lymphatic sheath, and B cells in the follicles/germinal centers
- marginal zone between where APCs present to lymphocytes
Mechanism of Class III antiarrhthmics
K+ channel blockers (Amidoarone, Sotalol)
- prolongs repolarization
- prolongs AP duration/ERP (end refractory period)/ QT interval
Pt w/ long-standing HTN presents w/ worsening renal fxn, biopsy of renal artery
(a) What stain is this?
(b) Dx
(a) PAS stain
(b) Hypertensive nephropathy- renal artery hyalinosis (deposits in arterial wall that cause thickening of arterial wall, causes subtype of atherosclerosis)
Pt w/ recurrent pyogenic infections, partial albinism, and peripheral neuropathy
-WBC on smear attached
Dx?
Dx = Chediak-Higashi Sydnrome
-WBCs w/ large granules
Chediak-Higashi = protein trafficking defect of impaired phagolysosome formation => increased risk of pyogenic infections (can’t destroy phagocytosed bacteria)
-giant granules in leukocytes are due to fusion of granules from the golgi
MC location of rhinosinusitis in adults
(a) MC cause
Rhinosinuisits = obstruction of sinus drainage into nasal cavity => inflammation and pain
-in adults MC in maxillary sinuses
(a) MC caused by viral URI, can be caused by superimposed bacterial
(a) Name these findings
(b) Dx
(a) Janeway lesions = small painless erythematous lesions on palms
- splinter hemorrhages
(b) 2 clinical manifestations of bacterial endocarditis
Dx
Most common primary cardiac tumor in adults = myxoma
-MC location is LA
Which lung cancer is this most likely?
Squamous cell carcinoma- hilar mass arising from the bronchus
-cavitation
Both squamous and small cell are the 2 lung cancers that are central (‘sentral’), squamous cell is the one that arises from the hilum and appears as a cavitation
Describe the structure of insulin
Preproinsulin –> proinsulin –> C-peptide + insulin
Insulin composed of alpha and beta chains held together by disulfide bonds
-C-peptide as marker of endogenously produced insulin
- coracoid process (scapula)
- clavicle
- R common carotid artery
- thyroid
- L internal jugular vein
- Clavicle (left)
- Subclavian vein (L)
- Humeral head (L)
- spine of scapula
- spinous process
Differentiate the two types of arteriolosclerosis
Arteriosclerosis = hardening of arteries, wall thickening and loss of elasticity
A- hylanosis- deposition of hyaline in intima of BV, caused by primary HTN and dibetes
B- hyperplastic where you get proliferation of smooth muscle cells from severe HTN
Explain the power of a study
(a) How to improve power
Power of a study = percent there is an association and the study finds that there is an association
H1 = alternative hypothesis- presence of association
H0 = null hypothesis- lack of association
(a) Improve power by increasing sample size
Describe the Hgb dissociation curve
(a) Name a few things that shifts it left
(b) Name a few things that shift it right
Hgb curve showing % of Hb saturation at a certain partial pressure of oxygen
(a) Shift left when Hgb has a higher affinity for O2, aka HbF (fetal), or in relaxed form (as it is in the lungs)
(b) Shift right in taut form when want to facilitate O2 unloading into tissues
- enhanced by H+, CO2, exercise, 2,3-BPG, altitude, temperature
Which lung cancer would show this histology
Keratin pearls seen in squamous cell carcinoma (RF: smoking)
Describe the difference in the V/Q matching at the apex vs. the base of the lungs
(a) How does this explain why Tb prefers the apex?
Apex (top) has a V/Q ratio of about 3, tons of wasted ventilation (much more O2 than blood flow)
- base has a V/Q ratio of .6, so higher blood flow (Q) than volume of air (V)
(a) Tb thrives in high O2 => flourishes in the apex, espect granuloma formations to prefer the apex
Differentiate positive and negative skew
Positive skew = result that drags tail to the right, mean > median
Negative skew = some smaller results/outliers that drag mean to the left: mean < median
Describe the structure of an antibody
(a) Light vs heavy chain
(b) Variable vs constant region
- Variable region contains both light and heavy chains, this is the part that recognizes antigens.
- Constant region determines the isotype/class and binds complement. Constant region is only heavy chain
- then have 2 disulfide bonds connecting heavy chains, and one disulfide bond on each side connecting heavy chain to light chain in the variable region
What side of the cell membrane is the ATP site of the Na/K ATPase
(a) Na in or out?
ATP site is on the cytosolic side
(a) 3 Na+ out for 2 K+ in
Mechanism of action (at the cellular level) of the following asthma drugs
(a) Albuterol
(b) Theophylline
(c) Ipratropium
(a) Albuterol = stimulates conversion of ATP –> cAMP, cAMP induces bronchodilation
(b) Theophylline (rarely used b/c of narrow therapeutic index)
(b) Ipratropium = muscarinic antagonist to prevent bronchoconstriction
5 mo old w/ recurrent bacterial infections
- uncomplicated birth but delayed separation of umbilical cord
- blood smear attached
Dx?
Dx =Leukocyte adhesion deficiency
Defect in LFA-1 integrin (CD18) protein on phagocytes => get neutrophilia (high neutrophils in serum) b/c neutrophils can’t escape the blood stream
- get absent pus formation at infection sites and impaired wound healing
- give away is delayed umbilical separation
40 yo M p/w episodic HA and palpitations/sweating
- BP 160/120
- plasma metanephrines elevated
(a) Dx
(b) Expected CT finding
(a) Dx = pheochromocytoma = nonmalignant adrenal medulla tumor secreting epi, norepi, and dopamine
(a) Name the CT finding
(b) Describe the pathology
(a) Ct finding = aortic aneurysm (local dilation in aorta)
- this one is abdominal (AAA) and suprarenal (above where renal artery branches off)
(b) 2/2 atherosclerotic buildup in aorta
Describe the structure of tRNA molecule
(a) 3’ end
(b) 5’ end
(c) Anticodon loop
tRNA = clover-shaped molecule w/
(a) 3’ end with 5’ - CCA - 3’ (always) that acts as amino acid receptor site
- CCA 3’ end gets covalently bonded to an amino acid by aminoacyl-tRNA synthetase
(b) 5’ end free
(c) Anticodon loop is what reads the mRNA codon
Briefly explain how antibody diversity is generated
- Random recombination of VJ (light chain) or VDJ (heavy chain) genes
- then random combination of heavy chains w/ light chains
- somatic hypermutation following antigen stimulation
- addition of nucleotides to DNA during recombination by terminal deoxynucleotidyl transferase
Describe the 3 ways in which CO2 is carried in the blood
90% is carried as HCO3- in RBCs, 5% is carried as dissolved in plasma, 5% is carried as HbCO2 (as bound to Hb)
Describe the process of elongation during protein synthesis
APE sites of ribosome:
- first tRNA binds to start codon (AUG) in P-site, bringing in methionine
- next tRNA enters A-site, ribozyme (rRNA) catalyzes formation of peptide bond, transfering growing polypeptide into the A-site
- ribosome advances 3 spaces towards the 3’ end of mRNA, moving tRNA into the P site until next tRNA comes along
Is this the right or left lung?
Pulmonary artery is anterior to the bronchus => it’s the R lung
RALS describes the relationship of the pulmonary artery to the bronchus: right anterior, left superior
What are lines of Zahn?
(a) Clinical significance
Lines of Zahn = interdigitating/alternating areas of pink (fibrin and platelets) and red (RBCs) in a clot formed pre-mortum
(a) Differentiate clots formed pre vs post-mortum
Differentiate PFT findings in obstructive vs. restrictive lung disease
Obstructive: marked scooping/sloping
Restrictive: very reduced volumes
Describe the main steps of thyroid hormone synthesis
- Iodine enters follicular cell, gets oxidized (by peroxidase) and pushed out into lumen as O2
- thyroglobulin synthesized in follicular cell pushed into lumen where it’s combined w/ I2, forming T3/T4 which gets re-endocytosed into follicular cell
- mostly released as T4 which peripherally gets converted into active form T3
Differentiate the 3 parts of the adrenal cortex
(a) What the secrete
(b) Regulatory system
Adrenal cortex: GFR, deeper you go the sweeter its gets
- Zona glomerulosa- secretes aldosterone (renin-angiotensin)
- Zona fasciculata- secretes cortisol (ACTH, CRH)
- Zona reticulata- secretes androgens (ACTH, CRH)
Explain how a test can be precise but not accurate
Precision = consistency/reproducability, while accuracy is validity/trueness of the response
-so a test can be precise if it consistently gets the same answer, but inaccurate if the answer isn’t the valid/correct one
Differentiate the 4 parts of Medicare
Part A = hospital insurance
Part B = paying the physicians, basic medical bills = doctor’s fees, diagnostic testing
Part C = A and B delivered by approved private companies
Part D = prescription drugs
Dx
Pleural effusion- note the hyperdense fluid btwn pleural layers in right lung
Differentiate centriacinar and periacinar emphysema
Centriacinar = associated w/ smoking (both pics)
Periacinar = alpha-1 antitrypsin deficiency
Describe the steps of the cell cycle
(a) M-phase vs. interphase
(b) 3 steps of interphase
Cell cycle: split into interphase and M-phase
(a) Interphase: 90% of cell life, split into G1 (growth), S-phase (synthesis), and G2
- M-phase = mitosis and cytolysis (splititng of cytosol)
(b) Interphase:
- G1 (growth)
- S-phase where new DNA material is synthesized, organelles are replicated (chromosomes become doubled)
- G2
-
Mechanism of Class II antiarrhythmics
Class II = beta-blockers
- decreases cAMP => reduces Ca2+ currents = suppresses abnormal pacemaker cells
- decreases slope of phase 4 depolarization and prolongs AV nodal repolarization
For SVT and rate control for AFib, Aflutter
See this Xray in a pt w/o atherosclerotic disease or peripheral artery disease
Dx?
Dx = Monckeberg atherosclerosis (rare) = medial calcific sclerosis = calcification of the elastic lamina of medium sized arteries
- so you get vascular stiffening w/o obstruction of blood flow
- so the arteries on CXR show up (b/c calcified) and are super huge-appearing, but flow is not obstructed b/c intima is not involved
Differentiate the histology btwn the two lung cancers shown
Left = small blue cells (neuroendocrine) cells of small cell carcinoma
Right = glandular pattern of adenocarcinoma
Formula for alveolar gas equation
PAO2 (alveolar) = 150mmHg - (PaCO2)/0.8
PaCO2 = arterial CO2
Describe the structure of cilia
(a) Result of dynein defect
Cilia structure: 9 + 2 microtubules (largest cytoskeleton fiber), doublets that slide on each other w/ an dynein (ATPase)
(a) Dynein defect = immobile cilia = Kartagener’s
C3 deficiency vs. C5-C9 deficiency
All 3 complement pathways diverge at C3- so need C3 to activate complement response, so C3 deficeincy presents early in life w/ overwhelming/recurring infection w/ encapsulated organism
-C5-C9 are needed to form MAC complex: present classically w/ recurrent infection w/ Neisseria meningitidis
Describe the mechanism by which low glucose and available lactose triggers lactose metabolism via the lac operon system in prokaryotes
Genes repsonding the the environemnt: when preferred energy source (glucose) is absent, and alternative lactose is available, alter gene transcription to activate lactose metabolism
- low glucose activates CAP (catabolite activator protein) which binds to DNA to stimulate transcription. Low gluocse stimulates adenylyl cyclase activity which increases cAMP from ATP, elevated cAMP activates CAP
- high lactose binds to repressor protein to remove it from the operator site
=> glucose absent and lactose available leads to transcription of genes used for lactose metabolism
Dx
Gingival hyperpigementation = buzzword clinical sign for adrenal insufficiency (primary)
-low cortisol => elevated ACTH which causes elevation of MSH (melanocyte stimulating hormone) as a biproduct => hyperpigmentation commonly seen in the mouth
Describe the Haldane effect that occurs to Hb dissociation curve in the lungs
In the lungs there is high O2, so O2 kicks H+ off the Hb molecule (high O2 promotes H+ dissociation from Hb) which promotes HCO3 formatuion –> CO2 + H20
-so in this way high O2 promotes CO2 formation (so we can exhale CO2!)
Differentiate two types of cardiomyopathy
A (left)= dilated cardiomyopathy- accounts for 90% of cardiomyopathies, sarcomeres are added in series so you see enlargement of cavities (ballooning of heart on CXR) and thinning of ventricular walls
B (right) = hypertrophic cardiomyopathy- see concentric hypertrophy of sarcomeres, thickening of septal walls, often hypertrophy is septal and can even become so severe as to cause outflow obstruction
Pathognomonic finding of asbestosis pneumoconioses
‘Ivory white’ calcified supradiaphragmatic and pleural plaques
Mechanism of class I antiarrhythmics
Class I = sodium channel blockers
- decrease the slope of phase O (of the fast opening voltage-gated Na channels)
- slows or blocks conduction
- state dependent: so selectively acts on tissue that is more frequently depolarized (aka in tachycardia)
= Quinidine, Procainamide, Dispyramide)
What is a Robertsonian translocation?
When the 2 long arms of acrocentric chromosomes (ones w/ centromeres towards the end) fuse and the short arms are lost
=> chromosomal imbalance
-can cause Downs and Patau syndrome
Mechanism of lipid lowering agents
(a) Cholestyramine
(b) Ezetimibe
(c) Gemfibrozil/fenofibrate
(d) Niacin
Lipid lowering agents
(a) Cholestyramine = bile acid resin, decrease bile acid resabsorption from intestines => liver must use more cholesterol to make more
(b) Ezetimibe = prevents cholesterol absorption at the brush border of the small intestines
(c) Fibrates upregulate lipoprotein lipase to increase TG clearance, also activates PPAR-alpha to induce HDL synthesis
(d) Niacin (vit B3) inhibits lipolysis (cholesterol –> VLDL) to reduce hepatic VLDL synthesis
6 week old M p/w lethargy and hypotonia
- jaundice w/ protruding tongue
- not born in a hospital :-(
Dx?
Dx = congenital hypothyroidism = cretinism
- MC 2/2 thyroid degenesis, can also be from iodine deficiency
- part of the newborn screening in the US
Differentiate the three activation pathways for complement
(a) Classic
(b) Alternative
(c) Lectin
(d) At what point do they all converge?
Complement activation by 3 pathways
(a) Classic pathway is due to antigen-antibody complex (by IgG and IgM)
- “GM” makes “classic” cars
(b) Alternative pathway is activated directly by microbial surface molecules
(c) Lectin pathway activates complement by mannose or other sugars on the microbe surface
(d) All converge at C3b
Formula for pulmonary vascular resistance
Well change in P = Q x R, so R = dP/Q
PVR = (Ppulm artery - Pleft atrium) / cardiac ouptut
Eukaryotic RNA processing
(a) Where does it take place?
(b) 3 steps
RNA is processed only in eukaryotes
(a) In the nucleus processed from hnRNA –> mRNA, then mRNA can leave nucleus into cytosol to be translated
(b)
- Add cap on 5’ end
- Polyadenylation (about 200 A’s) on 3’ end
- Splicing out introns and joining extrons
Describe the wya in which adaptive immunity cells (T and B cells) are activated by a foreign antigen
(a) Two-signal activation
(b) B7 and CD28
(c) CD40
- The naive T cells is activated by a dendritic cell (specialized APC that migrated thru the draining lymph node and presented antigen)
- dendritic cell presents antigen on MHCII to CD4+ (Th) cell and on MHCI to CD8+ (Tc) cell
- dendritic cell gives costimulatory signal by interaction of B7 and CD28
- then the activate T cells produces cytokines, Tc can recognize and kill virus-infected cells - TCR (T cell receptor) on CD4+ recognizes the MHCII from B cell (after B cell endocytoses foreign antigen)
- costimulation by CD40 on B cell binding to CD40 ligand (on Th cell)
- now Th cell releases certain cytokines to determine the Ig class switching of the B cell
Describe functional reserve capacity
FRC = amount left in lungs after normal exhale
FRC = RV (residual volume) + ERV (expiratory reserve volume)
What organ are Hassal corpuscles found in?
(a) Differentiate cortex and medulla
Thymus contains hassal corpuscles (function not fully understood)
(a) Cortex is densely packed w/ immature T cells, while medulla is pale and has few mature T cells
- thymus is encapsulated and separated into lobules
Dx and name of finding
Finding = xanthomas = plaques/nodules of lipid-laiden histiocytes that deposit on the skin, especially on the eyelids (called xanthelasma)
Dx = hyperlipidemia
Differentiate type I and type II error in outcomes of a statistical analysis
Type I error (alpha) = false positive error = you accept alternative hypothesis (that association exists) when null hypothesis is true (no relationship exists)
Type II error (beta) = false negative error = you say there is no assocation (accept null hypothesis) when an association exists (alternative hypothesis is true)
-1 - beta = power
What is housed w/in the 3 major components of a lymph node
(a) Follicle
(b) Medulla
(c) Paracortex
(a) Follicles contain the germinal centers that house B-cells
(b) Medullary cords hold tightly packed lymphocytes and plasma cells, medullary sinuses w/ reticular cells and macrophages
(c) Paracortex contains T cells- this is the part that enlarges during cellular immune response (ex: response to viral infection)
Describe the clinical features of acromegaly
Acromegaly 2/2 excess growth hormone in adults (typically 2/2 pituitary adenoma)
- large tongue w/ deep furrows, deep voice, large hands and feet
- coarse facial features (see pic)
- impaired glucose tolerance => diabetes
- increase risk of colorectal polyps and cancer
What is elastic recoil of the chest wall?
Elastic recol = tendency for the lungs to collapse inwards and the chest wall to move outwards
These are alveoli- name and explain the diagnosis
ARDS = acute respiratory distress syndrome
- clinical diagnosis of acute onset respiratory failure (often 2/2 pneumonia, sepsis, acute pancreatitis, uremia)
- vascular permeability => exudative (protein-rich) leakage => noncardiogrenic pulmonary edema
Effect of a defect in purine salvage
(a) What is the congenital syndrome called?
(b) Clinical features
(c) Tx
Defect in purine synthesis =>
(a) Lisch-Nyhan syndrome = aut recessive absent HGPRT enzyme => can’t salvage purines so they’re all shunted into uric acid
HGPRT:
(b) Hyperuricemia, Gout (also called juvenile gout), Pissed off (self-mutilation, aggressive), Retardation (ID), tonia (dystonic)
(c) Tx = allopurinol
Differentiate the symptoms of 17alpha-hydroxylase deficiency from 21-hydroxylase deficiency
17alpha-hydroxylase deficiency prevents production of both cortisol and sex hormones => all shunted towards aldo so very high aldo
-presents w/ ambiguous genitalia w/ undescended testes or lack of secondary sex characteristics
21-hydroxylase deficiency allows first step so you can’t make aldo but you can make sex hormones
-presents either in infancy w/ salt wasting (b/c low aldo) or in childhood w/ precocious puberty (high sex hormones)
Describe the function of NADPH in the immune system
Using reaction of NADPH –> NADP+ in phagolysosome, neutrophils and monocytes produce rapid oxidative species (ROS) used to kill ingested pathogens
What is produced by each of the 3 types of cells in the Islet of Langerhans?
(a) Contrast their locations
- Alpha cells (peripherally) produce glucagon
- Beta cells (centrally) produce insulin
- Delta cells (interspersed) produce somatostatin
How is it ensured that each tRNA carries a specific amino acid?
Matchmaker enzyme = aminoacyl-tRNA synthetase
- Aminoacyl-tRNA synthetase uses ATP to covalently bind CCA 3’ terminus of tRNA to a specific amino acid
- this step is what ensures the correct amino acid is added
- then this energy in the AA-tRNA bond is used to form a peptide bond in protein synthesis
Differentiate bacillary angiomatosis and Kaposi’s sarcoma
Hard to distinguish clinically, both seen in AIDS pts, both are tumors of vasculature
- bacillary angiomatosis benign- neutrophilic infiltrate
- Kaposis from HIV/HHV-8
Differentiate the 3 ways by which antibodies fight antigens
- opsonization- marking antigen for phagocytosis
- neutralization- prevent bacteria from adhering to endothelial surface
- activates complement to enhance opsonization and lysis
Where are T cells produced? Where do they mature (2 places)
T-cell precursors are produced in the bone marrow, then migrate to the thymus where the get receptors
- in the thymus they undergo positive vs. negative selection (apoptosis of ones that have too high an affinity for self antigens)
- then in lymph node CD4 helper T cells can respond to cytokines and differentiate even further
Differentiate the 3 vesicular trafficking signals used to communicate btwn rough ER, golgi, and plasma membrane
(a) COPI
(b) COPII
(c) Clathrin
Vesicular trafficking
(a) COPI for golgi-golgi transport, or cis-Golgi to ER (retrograde)
(b) COPII for ER to cis-Golgi (anterograde)
(c) Clathrin for trans-Golgi to lysosome, or plasma membrane to endosome (receptor mediated endocytosis)
Differentiate structure and fxn of type I vs type II pneumocytes
Type I: flat and thin (squamous) for optimal gas diffusion- makes up 97% of the alveolar surface area
Type II: cuboidal, secrete pulmonary surfactant
Curschmann spirals found in sputum- Dx?
Curschmann spirals = microscopic finding of desquamated epithelium in sputum seen in asthma
At the cellular level how does glucose stimulate insulin release from cells?
Glucose taken up by insulin-producing cells thru GLUT-2 and produces ATP which closes K+ channels to close => depolarizes cells which opens Ca2+ channels. Ca2+ influx stimulates insulin exocytosis
Function of DNA replication enzymes
(a) Helicase
(b) Single stranded binding proteins
(c) Topoisomerase
(d) Primase
(e) DNA ligase
(a) Helicase unwinds DNA at the replication fork
(b) Single stranded binding protein keeps the strands separated /prevents them from reannealing
(c) Topoisomerase create single or double-break stands in the helix to add or remove supercoils, aka breaks phosphodiestrase bonds to untangle DNA
(d) Primase makes an RNA primer on which DNA polymerase III can initiate replication
(d) DNA ligase joins Okazaki fragments (catalyzes formation of phosphodiesterase bond w/in a strand of dsDNA)
Describe the functional organization of a eukaryotic gene
(a) Enhancer
(b) Template vs. sense strand
(c) AT rich upstream sequence
Eukaryotic gene
(a) Enhancer region is where transcription factors (or even silencers) can bind- this region can be close or far from, or even in the introns of, the transcribed region
(b) Template strand is running 3’ to 5’ and coding strand is what mRNA reads from
(c) AT rich upstream sequence = promoter region close to transcribed region = where RNA pol II binds just upsstream of the gene locus (TATA box)
Describe the process of mRNA splicing
mRNA splicing (in the nucleus before it’s final): snRNP (small nuclear ribonucleoproteins) combine w/ pre-mRNA to form a splicesome
- then a lariat (loop) intermediate is generated
- lariat is released to simultaneously remove intron and join the two exons
Sidebar: it’s these snRNPs that are targed by anti-Smith antibodies in SLE
30 yo white F w/o PMH incidentally found to have BP of 180/100 on check up
Renal artery arterogram shows the following
Dx?
Dx = fibromuscular dysplasia (vasculopathy- non-atherosclerotic abnormal growth of arterial walls, especially renal and carotid)
- string on a bead appearance of the renal artery
- think of fibromuscular dysplasia as cause of secondary HTN in young F
Explain the benegit of Selegiline over Phenelzine
Selegiline = MAO-B selective inhibitor => mainly degrades DA (not NE and 5-HT) and leaves MAO-A available in teh gut to metabolize tyramine containing foods
So Selegiline doesn’t have the same dietary restrictions and risk of hypertensive crisis and nonselecitive MAO inhibitors
-less antidepressant effects, but very useful in adjunct to L-Dopa as Parkinsons tx
Differentiate abnormal passive abduction vs. adduction of the knee
Abnormal passive abduction = MCL injury
Abnormal passive adduction = LCL (lateral cruciate ligament) injury
Explain findings of McMurray test on knee exam
McMurray test: w/ pt supine internally and externall rotate knee
- pain/’popping’ on external rotation = medial meniscus tear
- pain/’popping’ on internal rotation = lateral meniscus tear
Unhappy triad of knee conditions caused by lateral blow to planted leg
Classically: damage to ACL, MCL, and medial meniscus (attached to the MCL)
What is a Baker’s cyst?
Fluid collection in the popliteal fossa, MC due to chronic joint disease
Bones of the wrist
‘So long to pinky, here comes the thumb’
Describe the sensation of the hand
Palmar surface: mostly median nerve w/ ulnar medially
Dorsal surface: radial and ular, then top of 2nd/3rd finger by median nerve
Which bands of the sarcomere shorten w/ muscle contraction
‘HIZ’ shorten: H-band (only thick myosin filaments), I-band (only thin actin filaments) and Z to Z distance (length of sarcomere) all decrease w/ muscle contraction
While A-band is the only one that stays the same!!! A is the full length of the myosin thick filament, doesn’t change w/ contraction
Explain how muscle depolarization causes Ca2+ release
Muscule depolarization travels down the T-tubule (extension of plasma membrane) and activates voltage-sensitive dihydropyridine receptors that are mechanically coupled to ryanodine receptors on SR
- Open ryanodine receptors = Ca2+ escapes out of SR into cytosol
- now tons of Ca2+ in cytosol to bind to troponin C and allow for contraction!
Explain why Ca2+ needs to be released from the SR for muscles to contract
Ca2+ needed to bind to troponin C, moving tropomyosin out of the way and exposing the myosin-binding groove on actin filaments
On a molecular level explain how NO causes smooth muscle contraction
Muscle contraction is all about actin/myosin
NO activates guanylyl cyclase, increasing intracellular cGMP which activates myosin-light-chain phosphatase
-dephosphorylated myosin is less active in contracting w/ actin => smooth muscle relaxation
Which bone cancers grow at the
(a) Epiphysis
(b) Metaphysis
(c) Diaphysis
(a) Epiphysis (above growth plate) = giant cell tumors
(b) Osteosarcomas grow at the metaphysis
(c) Ewings sarcoma and osteoid osteoma (benign) grow on the diaphysis
What kind of bone tumor?
(a) Histologic finding
‘soap bubble’ appearance on Xray = giant cell tumor
- at the epiphyseal end of long bones
(a) Multinucleated giant cells
What kind of bone tumor?
Cartilage outgrowth of the metaphysis of long bone = osteochondroma- benign tumor
-seen as mature bond w/ cartilaginous cap
Differentiate the appearance of the joint space in OA vs. RA
OA: joint space is narrowed w/ ulcerate cartilage and osteophytes
RA: increased synovial fluid enlarges joint space, bone and cartilage erosion w/ pannus formation
Which skin cancer?
Basal cell carcinoma (MC skin cancer) have “palisading” nuclei
Which skin cancer?
Squamous cell carcinoma of the skin (2nd MC behind basal cell carcinoma) w/ characteristic keratin pearls
Name of molecule that accumulates in the following lysosomal storage diseases
(a) Gaucher disease
(b) Niemann-Pick Disease
(c) Tay-Sachs
(a) Gaucher: glucocerebroside
(b) Neimann-Pick: sphingomyelin
(c) Tay-Sachs: GM2 ganglioside
