Renal

Drugs on this Prostaglandin Effect Example NSAIDs: aspirin, ibuprofen, methotrexate, naproxen

-Ibuprofin blocks prostaglandin synthesis -So now with mild sympathetic activity, prostaglandin synthesis is blocked which inhibits CYCLO-OXYGENASE -This causes increased constriction from both DIRECT & INDIRECT PATHWAYS leading to a larger decrease in Renal blood flow and a larger decrease in glomerular filtration rate

Glomerulotubular balance Ie. If you increase the GFR by 10%, you will also increase the reabsorption by 10%, called glomerular tubular balance.

-If GFR increases more NaCl & water is filtered and more NaCl and water is reabsorbed. -Glomerular filtration and tubular reabsorption is balanced. ~70% of filtered NaCl & water is reabsorbed even if GFR is increased Increased GFR does 3 things here: 1. Increases filtration of protein-free fluid -> Increases peritubbular capillary protein concentration -> Increased starling force for water & NaCl reabsortpion -> Increased NaCl reabsorbed 2. Increased filtration of glucose & amino acids -> Increased Na+ linked Tm reabsorption of glucose & amino acids -> Increased NaCl reabsorbed 3. Increased NaCl filtered -All of this leads to GLOMERULOTUBULAR BALANCE

Clinical value of blood urea nitrogen (BUN)

-If glomerular rate is reduced (e.g. halved), serum [creatinine] will double & [BUN] will double *i.e. BUN/creatinine ratio will be unchanged (normally ~15) -If patient is dehydrated, slight ↑ serum [creatinine], because slight ↓ GFR greater ↑↑ BUN, because slight ↓ GFR & ↑ urea reabsorption *i.e. the BUN/creatinine ratio will increase described as "pre-renal azotemia"

Na+ reabsorption: late distal tubule & collecting duct principal cells -Here the more Na you reabsorb, the more negative the tubular lumin get so therefore it is easier for K+ to be excreted -With High ADH, apical aquaporins are placed, and water would be reabsorbed. -Na+ reabsorption and K excretion is the action of ALDOSTERONE. It also increases the activity of the Na/K pump allowing the Na to go into the interstitial fluid (plasma)

-luminal membrane permeability to H2O depends on [ADH] -Na+ reabsorption & K+ secretion stimulated by ALDOSTERONE -site of action of K+ sparing diuretics *(spironolactone, amiloride, triamterene)

Palmar arches

-Radial artery and ulnar artery give rises to the superficial and deep branches in the hand -Superficial branches of the radial artery anastomose with the superficial branches of the ulnar artery making the SUPERFICIAL PALMAR ARCH -The deep branches of the radial artery anastomose wit the deep branches of the ulnar artery making the DEEP PALMAR ARCH - supplying the digital branches/digits. This is how the hand receives its blood supply

How to measure Urinary Flow Rate

-Units are in millimeters per minute -In the clinically, we do it based on 24 hour urines. They give them a bucket to pee in for 24 hours and then they bring it back for testing. They then do 60minutes x24 hours = 1440 minutes. If you are producing 1 mL per minute, then you will produces 1440 mL (1.44 L) which is relatively normal.

Edema: increased Pc (capillary blood pressure)

-Usually back pressure from VENOUS END of capillary -Autoregulation protects capillaries from ↑arterial pressure Left CHF -> Increased pulmonary vein blood pressure -> increased capillary pressure -> efflux of fluid from pulmonary capillaries to interstitial space (& ultimately into alveoli) Similarly: viral, alcoholic cirrhosis →↑ liver vascular resistance → ascites

Lateral ligament

-Weaker than the medial ligament and frequently injured -Stabilize the ankle joint during inversion of foot -Consists of three bands: 1. Anterior talofibular ligament 2. Calcaneofibular ligament 3. Posterior talofibular ligament

Sympathetic nervous activity (severe)

-When renal blood flow is severely reduced GFR will also be severely reduced because there is no blood to be filtered

Na+ reabsorption: early distal convoluted tubule This like a nice NISSAN. Na is driving, Cl is like a girlfriend (or a mistress smh) The actual job of diuretics is to block NaCl reabsorption

-luminal membrane IMPERMEABLE TO H2O ("cortical diluting segment") -tubular fluid becomes hypotonic (to 50-100 mOsm/kg water) -site of action of thiazide-like diuretics (hydrochlorothiazide, chlorthalidone)

Na+ reabsorption: thick ascending limb of loop of Henle -The TOYOTA CAMRY: The Na/K/Cl transport, has 4 binding sites. Na is driving, K+ is the passenger reading the maps, and the 2 kids, the 2 Cl-, are sitting in the back seat -On the basolateral surface, again the K/Na ATPase -The K+ tends to diffuse right back out of the cell here once it enters

-luminal membrane IMPERMEABLE to H2O ("diluting segment") -site of generation of medullary osmotic gradientNa+/K+/2Cl- transporter is site of action of loop diuretics *(furosemide, bumetanide, ethacrynic acid)

Regulation of Na+ excretion

Decreased blood volume -> Decreased arteriole blood pressure -> increased renin angiotensins aldosterone, and increased sympathetic nervous activity -> Decreased Na+ excretion Decreased blood volume also trigguers ATRIAL NATRIURETIC PEPTIDE to lead to decreased Na+ excretion *The decreased atrial natriuretic peptide and increased sympathetic nervous activity can also trigger an increase in renin, aldosterone and angiotensin

Shoulder Ligaments

1. Glenohumeral joint (shoulder joint): -Capsule -TRANSVERSE HUMERAL LIGAMENT---holds tendon of long head of Biceps -CORACOHUMERAL LIGAMENT -CORACOACROMIAL LIGAMENT 2. Acromioclavicular joint: -ACROMIOCLAVICULAR LIGAMENT -CORACOCLAVICULAR LIGAMENT— STRONGEST LIGAMENT -Helps the shoulder joint to be kept in place and also helpS us to transfer the weight from the clavicle to the shoulder joint

Regulation of plasma [Ca++]

Decreased plasma calcium -> Increased parathyroid hormone -> Increased calcium resorption, increased tubular calcium resorption, increased intestinal calcium absorption -> Increased plasma calcium

Renin release vs. afferent arteriole contraction

1. Juxtaglomerular Cells Increased cytosolic Ca2+ -> Inhibits adenylate cyclase -> Decreased cytosolic (cyclic AMP) -> Decreased renin release 2. Smooth Muscle Cells Increased cytosolic Ca2+ -> Ca2+ binds calmodulin -> Ca++ calmodulin activates myosin light chain kinase -> Muscle contracts, constricting afferent arteriole

Brachial Plexus: From the Lateral Cord

1. Lateral pectoral (C5,6,7): Pectoralis major - Adducts and medially rotates shoulder joint 2. Musculocutaneous (C5,6,7): Nerve of FLEXOR compartment of arm -The arm is divided as 2 compartiments (flexor and extensor) -Anterior - flexor compartment - most of which is innervated by the musculocutaneous nerve 3. Lateral root of median nerve

Body buffering: fixed acids

Addition of inorganic fixed acid or loss of HCO3- ~50%: buffered by extracellular HCO3- H+ + HCO3- -> H2CO3 -> H2O + CO2 ~50%: buffered by intracellular protein, phosphate, bone Take home message: addition of inorganic fixed acid increases extracellular [K+] Addition of organic fixed acid less increase in extracellular [K+] because H+ enters cell in undissociated form (e.g. H lactate)

Muscles of medial compartment of thigh

Adductor longus, Adductor brevis -Obturator nerve -Adducts thigh at hip joint Adductor magnus -Adductor part: Obturator nerve -Hamstring part: Sciatic nerve -Adductor part: Adducts thigh at hip joint -Hamstring part: extends thigh at hip joint Gracilis -Obturator nerve -Adducts thigh at hip joint Flexes leg at knee joint Obturator externus -Obturator nerve -Laterally rotates thigh at hip joint

Natriuretic peptides

Decreased blood volume -> Decreased arteriole blood pressure -> increased renin angiotensins aldosterone, and increased sympathetic nervous activity -> Decreased Na+ excretion Decreased blood volume also trigguers ATRIAL NATRIURETIC PEPTIDE to lead to decreased Na+ excretion *The decreased atrial natriuretic peptide and increased sympathetic nervous activity can also trigger an increase in renin, aldosterone and angiotensin

Sympathetic nervous system effects on Na+ excretion

Decreased systemic blood volume -> Increased sympathetic nervous activity -> 1. ALPHA 1 EFFECT - Decreased GFR -> Decreased Na+ filtered -> Na+ excreted ALSO, Alpha 1 effect has direct effect on tubular cells which -> Increases Na+ reabsorbed -> Decreased Na+ excreted 2. BETA 1 EFFECT - Increased Renin, Angiotensin, Aldosterone -> Increased Na+ reabsorbed -> Na+ excreted

Sodium balance -The body does not make sodium chloride

Experiment done on med students -Students started on a low sodium diet -You then increase sodium intake, and the kidney takes a little time to fully respond to this. On the first day it'll excrete about half of that, on the second, half of the remainder, on on the third day, half of the remainder of that then eventually the kidney will catch up -Then they go back on the low sodium diet, and the first day they are excreting more than they intake, but eventually it will match up -days 4-8: net positive Na+ balance = 140 mEq -> net H2O retention of 1L -days 9-22: body in Na+ balance as increased vascular volume -> Increased Na+ excretion -days 23-27: net negative Na+ balance = 140 mEq -> net H2O loss of 1L

Important principles 1

H+ secreted = HCO3- reabsorbed H+ excreted = titratable acidity + urinary NH4+ Most of the H+ secreted is used to "reclaim" filtered HCO3- Filtered HCO3- is not reabsorbed as such; it is destroyed in tubule and resynthesized in tubular cell New (net) HCO3- synthesized = H+ excreted = titratable acidity + urinary NH4+

Muscles of posterior compartment of the thigh These all originate from the ISCHIAL TUBEROSITY

Hamstring muscles: 1. Semi membranosus 2. Semi tendinosus 3. Biceps femoris 4. Hamstring part of adductor magnus Action: Flexors of the knee and Extensors of the hip Innervated by Sciatic nerve (tibial component)

Pathological conditions: chronic metabolic acidosis

chronic (several days) metabolic acidosis stimulates K+ secretion & excretion acute acidosis inhibits K+ secretion & excretion (previous slide)

Regulation: loop & thiazide diuretics -> Increased H+ secretion

loop & thiazide diuretics -> Increased H+ secretion, especially when K+ depleted

Pathological conditions: loop & thiazide diuretics

loop & thiazide diuretics stimulate K+ secretion & excretion

Urine osmolality & specific gravity

osmolality 50-1200 mOsm/kg 300 mOsm/kg specific gravity 1.003-1.030 1.010 Osmolality depends on molarity (i.e. number of particles) Specific gravity depends on mass (i.e. weight of particles) Generally, osmolality & specific gravity have linear relationship Exception: proteinuria (Increased mass, Decreased Molarity molarity) therefore specific gravity Increased disproportionately Modern labs generally use osmolalities

Renal plasma flow using p aminohippuric acid (pAH) -This is an infused substance

pAH properties 1. all pAH in filtrate enters tubule at glomerulus 2. (at moderate plasma [pAH]), all pAH in peritubular capillaries is actively secreted into the proximal tubule 3. therefore ~90% of renal plasma pAH filtered or secreted into tubule (i.e. is "cleared") *We don't measure the 5% that goes through the vasa recta and the 5% that goes through the perirenal fat/capsule Use of pAH to determine renal plasma flow 1. measure clearance of pAH 2. volume of plasma cleared = volume filtered + volume flowing through peritubular capillaries = 90% of total renal plasma flow 3. therefore: CpAH = ~90% of renal plasma flow (effective RPF) 4. CpAH/0.9 = true renal plasma flow

Body buffering: added bicarbonate

~50%: accumulates as extracellular HCO3- ~50%: H+ leaves cell and reacts with added HCO3- Take home message: addition of HCO3- lowers extracellular K+

Body buffering of daily fixed acid production

~70 mEq fixed acid produced metabolically each day reacts with 70 mEq extracellular HCO3- either directly, or after leaving intracellular buffering sites the kidney replaces the destroyed HCO3- (mechanism later)

Locking and unlocking of the knee

• Locking is a mechanism that allows the knee to remain in the position of full extension • Locking results from medial rotation of the femur on the tibia during extension •Unlocking of the knee occurs as result of lateral rotation of femur on the tibia at the beginning of the flexion •Popliteus muscle is responsible for unlocking of the knee

Gluteus Maximus -

•Arises from ilium, sacrum & sacrotuberous ligament and inserts to iliotibial tract (thickening of the fascia) & gluteal tuberosity •Innervated by INFERIOR GLUTEAL NERVE from the LUMBOSACRAL PLEXUS ( L5;S1,2) Action: • Acting from pelvis, it extends the flexed thigh. (climbing stairs, standing up from sitting position) • Lateral rotation of the thigh. • Upper fibers abduct the thigh. • The muscle is inactive during standing, bending forwards at the hip joint to touch the toes. • It is a tensor of the fascia lata, & through iliotibial tract it stabilizes the femur on the tibia when the knee extensor muscles are relaxed.

Plain radiographs

• Widely available • Reproducible • Patient friendly • 'Inexpensive' • Usually the indicated primary imaging modality • Consider the pathology in question-image the area in question • Supplemental views possible in most locations

Osteology of Hip All flexors of the legs are posterior EXCEPT for the hip

•Bony pelvis: Consists of two hip bones ,sacrum and coccyx •Hip bones articulate with sacrum to form sacroiliac joint (Plane synovial joint) •Two hip bones are united anteriorly by Pubic symphysis (Secondary cartilaginous joint)

Homeostasis of body K+: collecting duct flow

tubular flow -> Incrased K+ secretion & excretion tubular flow increases with diuretics & ECF volume expansion Mechanisms:

Primary aldosteronism (Conn's syndrome)

SEE RENAL PAPER NOTES!

Elbow Joint

-Hinge type of synovial joint -Articular surfaces: *CAPITULUM and TROCHLEA of humerus *Head of RADIUS and TROCHLEAR NOTCH of ULNA Movement: 1. Flexion - Brachialis & Biceps 2. Extension - Triceps and Anconeus

Quantitation of secreted H+ & reabsorbed HCO3-

"Titratable acidity" = excreted H2PO4- & other urinary buffers "Urinary ammonium" = excreted NH4+

MSK Radiology Outline

- Basic bone anatomy - ABCs: key features in assessing plain films - Interpreting in a clinical context - Common fractures and pathologies

Posterior Compartment of the Arm

-Radial Nerve (C5, C6, C7, C8, T1) 1. TRICPES BRACHII (lateral, medial and long heads) -EXTENSION of the arm *Note that the radial nerve also helps to supply the BRACHIALIS (anterior - flexor) muscle along with the MUSCULOCUTANEOUS NERVE

Blood supply of the knee joint -Popliteal artery gives off GENICULAR BRANCHES: Superior medial, superior lateral, inferior lateral, middle genicular, inferior medial genicular arteries -Before the femoral artery becomes the popliteal artery, it gives off a descending genicular artery and a descending genicular branch of the LATERAL CIRCUMFLEX ARTERY (which is a branch of the profunda femoris artery)

-(Anastomosis around the knee) • Five genicular branches of popliteal artery • Descending genicular branch of femoral artery • Descending branch of lateral circumflex artery • Anterior and posterior tibial artery The middle genicular artery is the only one that is not taking part in anastomoses -Superior medial w/ Inferior medial *Superior medial also has anastomoses desdcending genicular artery -Superior lateral w/ inferior lateral geniculary -*Superior lateral genicular w/ descending branch of the lateral circumflex -Anterior tibial recurrent artery (from the anterior tibial artery - which comes from the popliteal artery which divides into anterior and posterior tibial artery) anastomoses with the inferior lateral genicular. -Lower part of the femoral artery is blocked what anastomosis would work? The descending genicular arteries -Middle popliteal? All of the superiors anastomoses to the inferiors

Osteology of the foot

-7 tarsal bones -5 metatarsal bones -14 phalanges

Regulation: Increased aldosterone -> Increased H+ secretion

-> Increased H+ ATPase pump (-> intercalated cells) -> Increased H+ secretion -> Increased principal cell Na+ reabsorption -> more negative transepithelial potential difference -> Increased H+ secretion

Femoral hernia

-A protrusion of abdominal viscera(loop of bowel)through femoral ring into the femoral canal is called as femoral hernia -Seen as palpable mass below the inguinal ligament lateral to the pubic tubercle

The Arm

-ANTERIOR (FLEXOR) COMPARTMENT -> Musculocutaneous Nerve (C5, C6, C7) -POSTERIOR (EXTENSOR) COMPARTMENT -> Radial Nerve (C5, C6, C7, C8 and T1)

Popliteal cyst(Baker's cyst)

-Abnormal fluid filled sacs of synovial membrane in the region of the popliteal fossa -Generally cysts occur following previous injury, resulting in chronic knee joint effusion

Ankle(jerk) reflex

-Achilles tendon reflex is elicited by striking the tendo calcaneus briskly with a reflex hammer results in plantar flexion of the foot. -This tendon reflex tests the S1 and S2 nerve roots. -Both afferent and efferent of the reflex arc is carried by Tibial nerve

Movements at Metacarpophalyngeal joint( Condyloid joint)

-Adduction—palmar interossei -Abduction—dorsal interossei -Flexion—lumbricals and interossei -Extension—extensor digitorum, extensor indicis and extensor digiti minimi

Commonest injuries of the shoulder joint

-Anterior Dislocation of Humerus or Fracture at the surgical neck of the humerus -In this case, the pt's hx may be trauma and pain of the region -If you see this fracture you know that the AXILLARY NERVE (Root C5, C6 of the POSTERIOR CORD) is injured -The patient cannot ABDUCT over 15 degrees (deltoid muscle) -The patient will have some weakness with LATERAL ROTATION (teres minor) -The patient will have loss of sensation of the shoulder region

Muscular compartments of the leg

-Anterior compartment: Deep peroneal/Deep fibular nerve -Posterior compartment: Tibial nerve -Lateral compartment: Superficial peroneal/Superficial fibular nerve

Relations

-Anteriorly: Prepatellar bursa, Patellar ligament -Posteriorly: Popliteal vessels -Tibial and common peroneal nerves -Medially : Sartorius, semitendinosus and gracilis -Laterally :biceps femoris and tendon of popliteus

Arches of the foot

-Arches act as shock absorbers and they add to the weight bearing capabilities and resilience of foot -Medial Longitudinal Arch- formed by the calcaneus, talus, navicular, cuneiforms and the 3 medial metatarsals -Lateral Longitudinal Arch- calcaneus, cuboid and 4th & 5th metatarsals -Transverse Arch- runs from medial to lateral- formed by the cuboid, cuneiforms and base of metatarsals

Gluteus Medius and Minimus These support the pelvis of the opposite side

-Arises from outer surface of ilium and inserts to greater trochanter -Innervated by superior gluteal nerve(L5,S1) -Acting from pelvis: Abducts the thigh and anterior fibers rotate the thigh medially -Acting from femur: It supports the opposite half of the pelvis when the foot is off the ground

Forces of glomerular filtration

-At afferent arteriole end: *NFP = PGC - PBC - πGC = 60 - 15 - 28 = ~17 mm Hg Note: Bowman's capsule protein concentration is effectively zero. -Hydrostatic Pressure (Glomerular Capillaries): 60mmHg -Hydrostatic Pressure (Bowmans Capsule): 15 mmHg -Oncotic Pressure (Glomerular Capillaries): 28 -We have a net filtration pressure of about ~17 mmHg driving fluid through holes which are 100 times as dense as the muscle capillaries

Filtration forces along glomerular capillary

-At efferent end: PGC = 58 mm Hg, PBC = 15 mm Hg, πGC = 38 mm Hg -As you squeeze a protein free filtrate out of the plasma, the protein concentration left in the plasma continues to increase

Patellar tendon reflex Tests the femoral nerve -If there is injury to the femoral nerve, the pt cannot extend their knee and the pt will have weakned flexion of the knee

-Elicited by tapping the ligamentum patellae with a knee hammer -Positive response is the extension of the knee -Afferent limb- Femoral nerve -Efferent limb- Femoral nerve -Spinal center-(L2,3,4) -The reflex is lost when there is injury to femoral nerve or injury to spinal center

Arterial supply of upper limb

-Axillary artery starts at the 1st rib -Axillary artery then becomes the BRACHIAL ARTERY after the lower border of the TERES MAJOR -Brachial artery then bifurcates at the HEAD OF THE RADIUS into the ULNAR and RADIAL artery *The Brachial Artery also gives branch to the 1. PROFUNDA BRACHII which also gives rise to the RADIAL COLLATERAL ARTERY *Runs near the RADIAL NERVE posteriorly 2. SUPERIOR ULNAR COLLATERAL 3. INFERIOR ULNAR COLLATERAL -RADIAL ARTERY gives rise to the RADIAL RECURRENT BRANCH -ULNAR ARTERY gives rise to the COMMON INTEROSSEOUS ARTERY which then rise to the ANTERIOR INTEROSSEOUS ARTERY (deep artery of the anterior part of forearm) and POSTERIOR INTEROSSEOUS ARTERY (deep artery of the posterior part of forearm)

Glomerular filtration barrier Filtration slits: Coated with SIALOGLYCOPROTEIN *Can be stained with COLLOIDAL IRION Basement membrane: Includes CHONDROITIN-PROTEOGLYCAN *Can be stained with CATIONIC FERRITIN

-Barrier: *consists of mesh-like matrix of basement membrane and filtration slits -Charge configuration *basement membrane & filtration slits (not fenestrae) have net negative charge -The smallest protein in plasma is ALBUMIN and albumin has a negative charge as well. So when it comes to the filtration barrier, it will be repelled -This charge is very important because there are diseases where the charge barrier breaks down, in this case albumin will get filtered -Filtration slits: *coated with sialoglycoprotein (SGP in fig A) *stained with colloidal iron *filtration slit diaphragm is size-selective filter -Basement membrane: *includes chondroitin-proteoglycan ( *stained with cationic ferritin

Branches of Brachial Plexus: From The Roots

-Branch: DORSAL SCAPULAR NERVE *Root: C5 *Muscle: LEVATOR SCAPULAE (elevates the scapula) & RHOMBOIDS (retracts the scapula) -Branch: LONG THORACIC NERVE *Root: C5, C6, C7 *Muscle: SERRATUS ANTERIOR *Protracts the Scapula

Fracture distal end of Radius

-COLLE's FRACTURE of the wrist is a distal radius fracture in which the distal fragment is displaced (tilted) posteriorly, producing a characteristic bump described as DINNER (SILVER) FORK deformity because the forearm and wrist resemble the shape of a dinner fork -In the distal fragment is dipslaced ANTERIORLY, it is called a REVERSE COLLE'S FRACTURE (or SMITH FRACTURE) . This fracture may show styloid processes of the radius and ulna line up on a radiograph

Renal calcium handling 40% of Ca++ bound to albumin 60% unbound (50% is free ionized Ca, 10% is Ca kelated with citrate and phosphate and various things like that Therefore only 60% is filtered and virtually all of it is reabsorbed (LESS THAN 1% EXCRETED which is usually the 200mg that you are picking up from the GI tract everyday)

-Ca++ filtered: only the 60% not protein-bound is filtered -Ca++ reabsorbed: ~99% filtered load ( ~65% PT, ~25% TAL, ~9% distal), <1% excreted Reabsorption takes place mostly in: Proximal tubule: -mostly paracellular *Of the NaCl and water that is filtered at the glomerulus, about 2/3rds is reabsorbed form the proximal tubule. If the calcium that was filtered is not reabsorbed, as you reasorb the NaCl and water the calcium concentration would increase, ie only in 1/3 of the salt/water since some of the salt/water was reabsorbed. As the Ca concentration increases, it diffuses out of the tight junctions via a PARACELLULAR ROUTE. Paracellular route happens with Ca++ in the proximal tubule mostly due to the reabsorption of NaCl/Water, and as the Ca concentration rises it goes out through the tight junctions by simple diffusion But also in: THICK ascending limb: -50% paracellular, -50% transcellular *This has paracellular and TRANSCELLULAR REABSORPTION. *The transcellular route requires a calcium channel at the LUMINAL/APICAL membrane. It is very easy for calcium to go through that channel due to the steep electrochemical gradient (Ca concentration is roughly plasma levels in the TIL, and the Ca in the cell is very very low). Calcium comes in to bind with CALBINDIN (and CALCITRIOL stimulates the sysnthesis of calbindin). Once Ca is in the cell, you must do work to get it out of the basolateral membrane back into the blood. You would use 1. CALCIUM ATPase - Primary active transport (The same pump you use to get the Ca back into the SER when the muscle now is going to relax). 2. Ca++ Countertransport system - You expend 3 Na+ that come into the cell down its concentration gradient, and one Ca gets pushed out (You have to push calcium against the gradient so it takes 3 Na+ to do so). Distal tubule: -all transcellular -reabsorption stimulated by PTH which acts on luminal Ca++ channels) *REGULATION IS IN THE DISTAL TUBULE -That 9% that gets reabsorbed, it doesn't take very much change in the distal tubular reabsorption to alter that 1% excreted. It is very sensitive to little changes. If only 8% is reabsorbed here, then you would double the amount excreted. *Concerning the transcellular route that takes place in the distal tubule: If the intracellular sodium increases for any reason, then that is a less steep gradient for Na to come into the cell. Therefore anything that raises intracellular sodium in the distal tubule will inhibit the reabsorption of calcium. Anything that lowers sodium in the distal tubule cells will stimulate the reabsorption of calcium. -PTH acts in the DITAL TUBULE and acts on the tracellular Ca+ channel so Ca can enter the cell, and then the cell pumps it out through the basolateral surface -

Distribution of fluid between interstitial & vascular spaces

-Capillary endothelium is permeable to water, ions & small molecules -Water, ions & small molecules equilibrate across capillary endothelium (mostly by simple diffusion) -Capillary endothelium is minimally permeable to plasma proteins -Plasma protein remains in vascular bed, exerting osmotic (oncotic) pressure -This oncotic pressure tends to cause fluid to move from interstitial fluid to plasma -Capillary blood pressure tends to cause fluid to move from plasma to interstitial fluid -Pathological increase in interstitial volume is called edema -Controlled by "Starling forces" -where: *Pc = hydrostatic pressure of capillary (blood pressure) *πc = protein osmotic (oncotic) pressure of capillary *PIF = hydrostatic pressure of interstitial fluid *πIF = protein osmotic pressure of interstitial fluid -give each outward force a +ve sign, & inward force a -ve sign then: net pressure for efflux = +Pc - PIF - πc + πIF ARTERIAL END: -Pc = +35 mmHg -πc = -28 mmHg -PIF = -(-2) mmHg -πIF = +3 mmHg -Net pressure = +35 - (-2) -28 +3 = +12 mmHg VENOUS END: -Pc = +15 mmHg -πc = -28 mmHg -PIF = -(-2) mmHg -πc = +3 mmHg -Net pressure = +15 -(-2) -28 + 3 = -8 mmHg

Edema: increased πi (interstitial protein osmotic pressure)

-Cause: increased protein permeability of capillary endothelium →↑ πi. -Mediators of increased permeability include HISTAMINE and INTERLEUKIN -2 -Contributing factors: vasodilatation →↑ capillary b.p., →↑ fluid efflux Burns, inflammation, trauma -> release of vasoactive substances -> increased capillary permeability to protein (which leads to increased protein efflux into interstitial fluid) OR arteriolar dilation (which leads to incread blood flow & capillary pressure) -> Local Edema

Lateral ankle sprains

-Caused by excessive inversion of the foot with plantar flexion of the ankle -Anterior talofibular ligament is most commonly injured and calcaneofibular ligament may also be involved -Results in instability of ankle joint

Podocytes

-Cells in the kidney -These podocytes sit on the capillaries -It's cell bodies sit on bowmans space -The legs spread out and divide to form PEDECELLS -In between the pedecells is the FILTRATION SLITS (important in regulating what does and what does not get filtered)

Sodium chloride depletion effect on body water spaces

-Chronic sweating: loss of sweat but only replacing water -Adrenocortical insufficiency: failure to secrete aldosterone CHRONIC SWEATING or ADRENOCORTICAL INSUFFICIENCY -> NaCl depletion -> Decreased Plasma NaCl -> Decreased ECF Osmolality (along with decreased ADH & Decreased ECF volume) -> Water enters cells down osmotic gradient -> ICF volume increases AND ICF osmolality decreases

Wrist joint -The ulnar does NOT take part in this joint

-Ellipsoid type (or condylar type) of synovial joint -Articular surfaces: Lower end of radius with SCAPHOID and LUNATE bone -Movements: Flexion - Flexor carpi radialis, Flexor carpi ulnaris and Palmaris longus Assisted by Flexor digitorum superficialis and Profundus Extension -Extensors of the forearm except supinator Abduction- Flexor carpi radialis and extensor carpi radialis longus and brevis Adduction- Flexor carpi ulnaris and extensor carpi ulnaris

Pott fracture-dislocation of ankle

-Excessive forcible eversion causing horizontal fracture of medial malleolus and oblique fracture of shaft of fibula & also lateral malleolus with tear of deltoid ligament. -It occurs when the foot is caught in the rabbit hole in the ground & the foot is forcibly everted.

Radial Nerve Skin of the posterior arm, forearm and hand all innervated by the RADIAL NERVE

-Comes from the POSTERIOR CORD of the BRACHIAL PLEXUS -Roots are C5, C6, C7, C8, T1 -Passes through the TRIANGULAR SPACE -Runs in the RADIAL (SPIRAL) GROOVE *On the posterior aspect of the humerus *It is also passing with the PROFUNDA BRACHII ARTERY (DEEP BRACHIAL ARTERY) In the AXILLA gives branches to the 1. LONG HEAD OF TRICEPS 2. MEDIAL HEAD OF TRICEPS 3. POSTERIOR CUTANEOUS NERVE of the ARM In the SPIRAL GROOVE it gives branches to the: 1. LATERAL HEAD OF TRICEPS 2. MEDIAL HEAD OF TRICEPS 3. ANCONEUS 4. LOWER CUTANEOUS NERVE of the ARM 5. POSTERIOR CUTANEOUS NERVE of the FOREARM In the ELBOW REGION: supplies the ELBOW JOINT In the ARM it gives branches to: 1. BRACHIALIS (which has dual innervation from the radial nerve and the musculocutaneous nerve) 2. BRACHIORADIALIS 3. EXTENSOR CARPI RADIALIS LONGUS In the CUBITAL FOSSA it gives branches to the TERMINAL BRANCHES (Superficial which is sensory, and deep which is muscular) *The superficial branch travels all the way down and it innervates the skin on the dorsum of the hand on the lateral side, as well as the proximal side of the fingers on the lateral side *The deep branch is called the POSTERIOR INTEROSSEOUS NERVE which innervates all the other extensors of the forearm

Scaphoid Fracture

-Commonly fractured of the carpals -Also common in fall with outstretched hand (can cause clavicle fracture, colle's fracture, and scaphoid fracture) -Here you would palpate the anatomical snuff box during exam, if there is tenderness then the pt has a scaphoid fx -Complication is AVASCULAR NECROSIS of the scaphoid bone *The radial artery is supplying the distal portion of the scaphoid bone, if there is a fracture at this bone it will block the supply to the proximal side of the scaphoid bone leading to avascular necrosis

Varicose veins

-Commonly seen in people whose job requires prolonged standing Etiology: Incompetent(diseased) venous valves Signs: •bulging/dilated veins •Leg swelling Complications: Venous stasis -> Discoloration of skin -> Venous ulcers

Axillary Artery

-Continuation of the SUBCLAVIAN ARTERY -The axillary artery extends from the the outer border of the FIRST RIB until the lower border of TERES MAJOR -After the Teres Major, the axillary artery turns into BRACHIAL ARTERY -The PECTORALIS MINOR muscle divides the axillary artery into 3 PARTS

Countercurrent multiplier: urea gradient Urea gradient is highest in the deepest part of the medullary interstitium, and lowest in the cortical region -It depends on the collecting duct -In the presence of ADH, the collecting duct is permeable to water -As it comes out of the distal tubule, the tubular fluid is hypotonic. If you make the collecting duct permeable to water, it will go from dilute tubular fluid to isotonic cortical interstitium. -In the presence of ADH, the entire collecting duct is permeable to water UREA IS DIFFERENT. COrtical and outer medullary collecting duct is PERMEABLE TO WATER and IMPERMEABLE TO UREA. As you reabsorb water, the urea concentration will increase. The urine will continue to concentrate and the concentration of urea increases as it goes to the outer medulla then the inner medulla. Just before the urea thinks its getting to be the urine, it is reabsorbed because the inner medullary collecting duct is PERMEABLE TO WATER, and PERMEABLE TO UREA due to ADH. *This is how you raise the BUN in dehydrated patients -The urea will diffuse out down its concentration gradient out of the tubule. Then it will diffuse out into the cortex down its concentration gradient

-Cortical & outer medullary collecting duct permeable to water, impermeable to urea water reabsorbed, [urea] increases -Inner medullary collecting duct permeable to water, permeable to urea -urea reabsorbed down gradient ADH -> Increased urea permeability

Edema Leads to block of lymph flow

-Definition: pathological increase in the volume of the interstitial fluid space -Usually caused by disruption of Starling forces -↓ πc plasma protein osmotic pressure (e.g. liver disease, nephrotic syndrome) -↑ πIF secondary to ↑capillary protein permeability (e.g. burns, trauma, infection) -↑ Pc capillary pressure (e.g. left heart failure, cirrhosis → hepatic portal hypertension) -blockage of lymph flow (e.g. filariasis, lymph node removal)

Bowleg (genu varum)

-Deformity in which the tibia is bent medially -May occur as a result of collapse of the medial compartment of the knee and rupture of the lateral collateral ligament.

Knock-knee (genu valgum)

-Deformity in which the tibia is bent or twisted laterally -May occur as a result of collapse of the lateral compartment of the knee and rupture of the medial collateral ligament

Popliteal fossa (You dont have to memorize the boundaries, only for your orientation)

-Diamond shaped intermuscular space at the back of the knee -Boundaries: -Superiorly-biceps femoris, semitendinosus and semimembranosus muscles -Inferiorly -2 heads of gastronemius and plantaris -Roof-skin and fascia -Floor-Popliteal surface of the posterior surface of the FEMUR, joint capsule and popliteus muscle

Fracture lower end of radius

-Distal fracture of radius with posterior displacement- Colles fracture---causes dinner fork deformity -Distal fracture of radius with anterior displacement- smith's fracture

Movements of the ankle joint

-Dorsiflexion: Tibialis anterior, Extensor hallusis longus, Extensor digitorum longus and peroneus tertius -Plantarflexion: Tendo-calcaneus, Tibialis posterior ,Flexor digitorum longus and Flexor hallucis longus

Water, D5W, or SIADH on body water spaces

-Drinking water -D5W is shorthand for a 5% W/V DEXTROSE (GLUCOSE) solution -SIADH (syndrome of inappropriate ADH secretion) is unregulated release of ADH, usually from a tumor *High ADH causes water retention in the body 5% W/V GLUCOSE given IV -> Glucose is metabolized to OSMOTICALLY INACTIVE PRODUCTS (ie LIVER GLYCOGEN) -> ingested water enters ECF (therefore ECF volume increases, ECF osmolality decreases, AND high ADH stimulates water reabsorption) -> Water enters ICF (cells) down osmotic gradient -> ICF volume increases & ICF osmolality decreases

Pain without trauma: Calcaneal Spur

-Due to inflammation of Plantar aponeurosis -Seen with chronic inflammation to the plantar fascia/aponerurosis because of abnormal bone growth from attachment sight of plantar fascia and calcaneal bone -Can suggest wearing smooth foot wear -Supportive treatment

Glomerular Structure

-Has an OUTER LAYER and INNER LAYER -Inner layer lies the capillaries of the glomerulus *Inner layer has PODOCYTES

Fractional excretion of sodium (FENa+) - calculation

-FENa+ = Na+ excreted/Na+ filtered (usually expressed as percentage) -Na+ excreted = V x UNa -Na+ filtered = GFR x PNa = (Ucreat x V /Pcreat) x PNa -So: FENa+ = Na+ excreted/Na+ filtered x 100% = (V x UNa) x (Pcreat/Ucreat x V) x (100%/PNa) = (UNa x Pcreat x 100%) / (PNa x Ucreat) -V (flow rate) cancels, and analysis done on single blood & urine samples -Normal FENa+ = 0.5% (i.e. 99.5% filtered Na+ is reabsorbed)

Colle's fracture

-Falling on the outstretched hand can also injure the lower end of the radius -You can't really appreciate if it is displaced anteriorly or posteriorly in an AP view so you also take a lateral view -Colle's fracture the distal portion of the radius is displaced posteriorly (dinner fork deformity) -Smiths fracture the distal portion of the radius is displaced anteriorly

Kidney Definition

-Filtration: movement of ultrafiltrate of plasma into Bowman's space (no proteins) *Technically only 20% of plasma is filtered into the Bowman's Space (Ie, therefore 20% of glucose would be filtered) *Afferent flow is 100%, filtration is 20% and efferent flow is 80% -Reabsorption: movement of water & solutes from tubule to peritubular capillaries *MOSTLY everything is reabsorbed -Secretion: movement of water & solutes from peritubular fluid to tubule -Excretion: removal of substances from body in urine Hence: Excretion = Filtration - Reabsorption + Secretion

Movements of the shoulder joint & the muscles producing them

-Flexion: Pectoralis major, anterior fibers of deltoid, coracobrachialis, biceps brachii -Extension: Posterior fibers of the deltoid, teres major, latissimus dorsi -Medial rotation: Anterior fibers of deltoid, pectoralis major, teres major, subscapularis, latissimus dorsi -Lateral rotation: Infraspinatus, teres minor & posterior fibers of the deltoid -Adduction: Pectoralis major, teres major, latissimus dorsi, anterior fibers of deltoid -Abduction: (0-15degrees) Supraspinatus, (15-110degrees) middle fibers of deltoid and (110-180degrees) Serratus anterior and trapezius

Movement at the Interphalangeal Joint (Hinge Joint)

-Flexion—flexor digitorum superficialis (proximal interphalangeal joint), flexor digitorum profundus (distal interphalangeal joint) -Extension—lumbricals and interossei (when metacarpophalangeal joint is extended by extensor digitorum) -Extension—extensor digitorum (when metacarpophalangeal joint is flexed by lumbricals and interossei)

Angiotensin II on afferent & efferent arterioles

-For slight increases in Ang II concentration *efferent arteriole constriction > afferent arteriole constriction *GFR increased; RBF reduced For high concentrations of Ang II *afferent and efferent arterioles are severely constricted *GFR & RBF are both reduced

Brachial Plexus

-Formation: It is formed by the VENTRAL RAMI of the lower four cervical and first thoracic nerves (C5, 6, 7, 8 and T1) -Pre & Post fixed conditions: Contribution from C4 nerve constitutes 'PRE-FIXED CONDITION' of the brachial plexus and contribution from T2 nerve constitutes 'POST-FIXED CONDITION' of the brachial plexus Parts : -SUPRACLAVICULAR PART (Roots & trunks) -INFRACLAVICULAR PART (divisions, cords, branches) -The brachial plexus travels between the SCALENE MUSCLES -Once they arise from the roots in the neck, they make the TRUNKS coming together and travel through the SUBCLAVAIN TRIANGLE in the neck - THIS IS THE SUPRACLAVICULAR PART (roots, trunks) -Divisoins, cords and branches of the brachial plexus comprise the INFRACLAVICULAR

Boxer's Fracture Dislocation

-Fracture dislocation of 5th metacarpal

Fracture of the femur neck

-Fracture here can injure the Common fibular nerve injuryed -Foot drop! -They cannot do eversion also because of the superficial fibular part of the common fibular nerve -Sensations of the dorsum of the foot is entirely lost

Common sites of Compressin of Ulnar Nerve

-Fracture of the MEDIAL EPICONDYLE could injure the ULNAR NERVE -Called CUBITAL TUNNEL SYNDROME -As you try to flex the hand it will deviate laterally (because of flexor carpii radialis), there will be deformity with the fingers because of the lumbricals of the ring and index finger are paralyzed (flexion at the metacarpal phalyngeal is reversed to extension, and extension of interphalynges will become flexion - called ulnar claw hand), medial 1 and 1/2 fingers and medial aspect of the palm would lose sensation -Fracture of the HAMATE BONE could injure the ULNAR NERVE -Injury to GUYON'S CANAL could injure the ULNAR NERVE -Here the nerve will get trapped as it is traveling to the hand -This usually happens with bycycle riders - also called HANDLE BAR PALSY -Pain in the hand/forearm, Sensory changes on the little finger and ring finger (loss of sensation or tingling), weakness or wasting of intrinsic muscles of the hand will lead to claw posture of the hand

Shoulder joint

-GLENOHUMERAL JOINT - Ball and socket type of synovial joint *Between the GLENOID FOSSA and the HEAD OF THE HUMERUS -ACROMIOCLAVICULAR JOINT - Plain synovial joint *Between the CLAVICULAR PROCESS and ACROMION PROCESS -Ball and socket synovial joint, multi axial joint

Carpal Tunnel Syndrome

-If the synovial sheath around the tendon passing in the carpal tunnel gets swollen (common in females with hormonal changes) it will press on the median nerve passing through -This can also be caused by dislocation of a carpal bone (commonly the LUNATE) which compresses the median nerve -Everything seen in the wrist level injury would be present EXCEPT PALMAR SENSATION because the PALMAR CUTANEOUS NERVE goes ABOVE the RETINACULUM You test for carpal tunnel by: 1. Tapping at the wrist level around the course of the median nerve, if the patient feels pain and tingling then it is TINEL'S SIGN -You can also ask the patient to flex to wrist at 90 degrees for 30-60 seconds, if there is recurrent pain then it is another confirmitory test for median nerve compression in the carpal tunnel (POSITIVE PHANEL'S MANEUVER)

Course of the Median nerve

-In the AXILLA: No branches will be given from the median nerve -In the ARM: It gives branches to the artery (VASCULAR BRANCH) and the elbow joint (ARTICULAR BRANCH) *Does NOT give off MUSCULAR or CUTANEOUS branches here -In the ELBOW: It goes through the CUBITAL FOSSA - MEDIAL to the BRACHIAL ARTERY but gives off no branches -In the FOREARM: It passes through the PRONATOR TERES to enter the forearm and then it passes through the FLEXOR DIGITORUM SUPERFICIALIS and FLEXOR DIGITORUM PROFUNDUS *Here it will give branches to all the FLEXOR MUSCLES of the FOREARM - Pronator teres, flexor carpi radilis, flexor carpii ulnaris, Palmaris Longus, Flexor digitorum superficialis *It also gives a DEEP branch called the ANTERIOR INTEROSCIOUS NERVE which innervates the Flexor digitorum profunds for 2nd & 3rd digit, flexor policis longus, and pronator quadratos -At the WRIST: Before entering the wrist and hand, it gives off the PALMAR CUTANEOUS NERVE which travels ABOVE the FLEXOR RETINACULUM which innervates the LATERAL PART OF THE PALM *The median nerve then passes underneath the FLEXOR RETINACULUM in the CARPAL TUNNEL (where the flexor retinaculum attaches to the carpal bones, SCAPHOID and TRAPEZIUM laterally, and HOCKAMATE and FISIFORM BONE, making a tunnel) -The median nerve passes through the tunnel and enters the palm -In the PALM: It immediately gives off a branch to the thumb side called the RECURRENT BRANCH of the MEDIAN NERVE innervating the THENAR MUSCLES of the THUMB. The Median nerve further continues and gives 2 branches for the 1ST and 2ND LUMBRICALS. Then it also gives the CUTANEOUS branch innervating the skin of the 3 and 1/2 fingers on the PALMAR SIDE, and just the FINGER TIPS of the THUMB, INDEX & MIDDLE HALF OF INDEX FINGER on the DORSAL SIDE!

Serratus Anterior

-Innervated by the LONG THORACIC NERVE -Action: PROTRACTION of the scapula & also helps in overhead abduction -Long thoracic nerve runs superficially to and innervates the serratus anterior -This nerve can be injured in a RADICAL MASTECTOMY. -Testing of the muscle: The person is asked to place the stretched hands on the wall & push forwards. Normally the scapulae will remain fixed to the thoracic cage. If medial border of scapula lifts off of the chest wall when pushed against resistance it is indicative of weakness or paralysis of the serratus anterior. Called a POSITIVE WINGING OF THE SCAPULA SIGN

Inulin Used to find GLOMERULAR FILTRATION RATE

-Inulin is a polysaccharide that is administered instead of PAH. -Inulin is ONLY filtered so when we take the clearance formula and measure the urine concentration of inulin x urine flow rate / plasma concentration of inulin we get GFR -Creatinine is the breakdown product of CREATIN which is an amino acid known as CREATIN PHOSPHATE and we have CREATIN PHOSPHATE KINASE (CPK) -Creatin gets broken down all the time to creatinine and gets excreted. -We have an endogenous substance that is 90% filtered and 10% secreted (good thing to check filtration rate but only 90% effective) -If the plasma creatinine is HIGH we expect Glomerular Filtration Rate to be low if all of the other factors are normal *This is because if it is high in the plasma, he knows it is NOT being cleared very well

Inversion & Eversion

-Inversion is performed by Tibialis anterior and Tibialis posterior -Eversion is performed by Peroneus longus, Peroneus brevis and Peroneus Tertius

Isotonic saline or Ringers lactate on body water spaces

-Isotonic saline: 0.9% NaCl (~300 mOsm/kg water) -Ringers lactate: Na+, Cl-, K+, Ca++, & lactate- (generates HCO3-) ISOTONIC SALINE enters the ECF -> Solute stays in ECF (ECF volume increases but ECF osmolality stays the same) -> No osmotic gradient so no water flux (ICF stays the same, ICF osmolality stays the same)

Sciatic nerve Seen below the piriformis muscle running in the gluteal region. It runs all the way down in the back of the thigh and at the upper part of the popliteal fossa, it terminally divides as the tibial nerve and the common fibular nerve Before it splits, the sciatic nerve has 2 components. Tibial part of the sciatic nerve is supplying the muscle of the back of the thigh, but only the short head of the biceps is receiving its innervation from the common fibular component of the sciatic nerve. THen at the upper part of the popliteal fossa it properly divides as the tibial and common fibular nerve

-Largest nerve of the body (L4-5,S1,S2 and S3) -Exists the pelvis via greater sciatic foramen below the Piriformis muscle -Branches: Muscular branches 1. Semi tendinosus 2. Semi membranosus 3.Long head of biceps femoris 4.Hamstring part of Adductor magnus -Articular branch-Hip joint -Terminal branches 1.Tibial nerve (L4-S3) *Tibial nerve supplies the muscles at the back of the leg 2.Common peroneal(fibular)nerve (L4-S1) -Divides deep and superficial fibular, supplying the muscles of the lateral and anterior compartment of the leg

*Lateral collateral tendon does not have any attachment to the LATERAL MENISCI *When you see the medial collateral ligament, it is attached to the femur and the tibia and it also has an attachment to the medial meniscus -If there is any injury of the medial collateral ligament it is most likely due to the LATERAL BLOW of the knee. It may also injury the medial meniscus also because of its attachment to it

-Lateral collateral ligament: Cord like structure -Attachment: above-lateral condyle of femur Below-head of the fibula -Popliteus muscle intervenes between the tendon and lateral meniscus -Medial collateral ligament: Flat band like structure -Attachment: above-medial condyle of femur -Below-medial surface of shaft of the tibia -Firmly attached to the medial meniscus -Oblique popliteal ligament: -Strengthens the posterior aspect of the capsule -Derived from the semi membranosus tendon

Contents in Axilla (Lymph Nodes) -Breast cancer can metastasize to the PECTORAL GROUP of axillary lymph nodes

-Lateral: HUMERAL LYMPH NODES -Posteriorly: SCAPULAR LYMPH NODES -Anteriorly: PECTORAL LYMPH NODES -All 3 types of axillary lymph nodes drain into CENTRAL LYMPH NODES which drain into APICAL LYMPH NODES which drain into SUPRACLAVICULAR LYMPH NODES, which then goes into their respective lymphatic duct (right - right lymphatic duct, left - thoracic duct) then it goes to the venous channels Humeral/Scapular/Pectoral Axillary Lymph Nodes -> Central Lymph Nodes -> Apical Lymph Nodes -> Supraclavicular Lymph Nodes -> Right Lymphatic Duct/Thoracic Duct -> Venous Channels -Breast cancer can metastasize to the PECTORAL GROUP of axillary lymph nodes -Upper limb infections MOSTLY go into HUMERAL LYMPH NODES (then they travel to central, apical, supraclavicular, and so on) -Any injury of the axilla will hit the AXILLARY VEIN first. More than bleeding there, if there were a cut we would be worried more about air being sucked in causing an AIR EMBOLISM -The axillary vein drains into the SUBCLAVIAN VEIN which then joins with the INTERNAL JUGULAR VEIN to form the BRACHIOCEPHALIC VEIN which will then become the SUPERIOR VENA CAVA *Therefore any venous air emboli can travel this pathway which could be deadly *Cut to axillary vein leads to air embolus that travels from Axillary vein -> Subclavian vein (which joins with Internal Jugular Vein) -> Brachiocephalic Vein -> Superior Vena Cava

Medial ankle sprains

-Less Common -Caused by excessive eversion -Fibers of deltoid ligament torn -At times, the deltoid ligament pulls the medial malleolus thereby causing avulsion fracture of medial malleolus

Major Ligaments supporting the Arch

-Long Plantar Ligament- from calcaneus to cuboid. -Calcaneonavicular "spring" Ligament- from sustentaculum tali to the navicular. Ligament has many elastic fiber providing "spring" or stretch support for the overlying talus (supports the head of the talus) -Plantar aponeurosis

Na+ reabsorption: early proximal tubule

-Low Na+, Na+/K+ ATPase -Steep electrochemical gradient for sodium to come into the cell -Much of sodium enters with Tm substances -There is also a Na+/H+ countertransport system

Important Bony Landmarks

-Lower end of the femor has condyles (MEDIAL and LATERAL CONDYLES) -In front of the lower femur is the patellar bone (sesamoid bone) -In the lower leg there are 2 bones, Medially there is the tibia, laterally there is the fibula -The Tibia has a bony projection - tibial tuberosity - attachment of ligamentum patellae -Lower part of tibia has medial malleolus -Lateral malleous is on the lateral portion of the fibula -The superior surface of the tibia has 2 articular areas where the femoral condyles sit making the knee joint -Posterior and anterior intercondylar area is where the intercapsular ligaments attach

Klumpke's paralysis

-Lower/Inferior trunk injury, C8 and T1 (Klumpke's paralysis) -Causes: Undue abduction of arm (as in clutching something with hands after a fall from a height, during a difficult breech delivery (birth palsy or obstetric paralysis), by a cervical rib (cervical rib syndrome), or by abnormal insertion or spasm of the anterior and middle scalene muscles (scalene syndrome) or fracture clavicle -Deformity: Claw hand is an extension at the metacarpophalangeal joint and flexion at the inter- phalangeal joints. -Paralysis of intrinsic muscles of hand supplied by C8 and T1( lower trunk) nerves

Modulating role of prostaglandins -Both the Direct and Indirect effect are mediated by the IP3 system. -When IP3 production is increased, renal prostaglandin synthesis is increased (because IP3 there is a glycerol molecule, fatty acid, second fatty acid in the middle position , and a inositol bisphosphate hooked on to the phosphate group. The middle fatty acid is usually ARACHIDONIC ACID which is a fatty acid with four double bonds and is a precursor for prostaglandin synthesis). At the same time that you are constricting the afferent and efferent arterioles you are also producing prostaglandins in the kidneys

-Mild cardiac impairment -> increased sympathetic nervous system activity -> A. DIRECT EFFECT: Afferent constriction GREATER THAN efferent constriction -> Decreased Renal blood flow & decreased GFR B. INCREASED RENIN, ANGIOTENSIN II -> efferent constriction GREATER than afferent constriction -> Decreased renal blood flow & increased glomerular filtration rate -Both A & B cause increased renal prostaglandin synthesis which leads to renal vasodilation that modulates the afferent and efferent constriction leading to the decreased renal blood flow & decreased glomerular filtration rate -The prostaglandins say "Okay, you can constrict, but don't go overboard -Prostaglandins: PGE2 & PGI2 (prostacyclin) from arachidonic acid in 2 postion of phosphatidyl inositol bisphosphate

Sympathetic Nervous System Effect on the Kidney *Note: afferent constriction = efferent constriction, *GFR ↔, RBF ↓, ∴↑ filtration fraction (GFR/RPF)

-Mild vs Severe *If you lose a L of blood, you will fire your sympathetics hard and it will be a severe response *If you are a little nervous about an exam coming up, thats mild sympathetics and is a subjective situation Mild Sympathetics will cause: -Partial constriction of the AFFERENT arterioles and partial constriction of the EFFERENT arterioles *If you just constricted the afferent arteriole, both RPF and the glomerular capillary pressure would fall *If you just constricted the efferent arteriole, GFR would increase and the RPF would decrease (because you've increased the resistance and this will cause a decrease in flow) -If you just gave both the afferent and efferent arterioles a gentle squeeze, you maintain the glomerular capillary pressure & GFR but RPF would fall because you've constricted both and increased the resistance to kidney to plasma flow *If you squeeze the afferent the glomerular capillary pressure would go down so GFR would go down. If you then squeeze the efferent, the glorular capillary pressure would go back up again. So by lightly squeezing both of them you keep the glomerular capillary pressure constant therefore GFR constant. RPF however would fall! Here you increased the Filtration Fraction (you are filtering more, going from like 20% to 25%) because you are getting the same GFR out of a reduced RPF so the filtration fraction increases

Charge selectivity of glomerular filtration barrier

-Minimal change nephropathy: -nephrotic syndrome 2° to loss of negative charges of filtration barrier (with little histological changes)

Dislocation of the Hip joint

-Posterior dislocations are most common: Occur during an automobile accident when the hip isflexed, adducted, and medially rotated. Posterior dislocation can result in injury to sciatic nerve. This result in paralysis of the hamstrings and muscles distal to the knee supplied by the sciatic nerve. Sensory changes may also occur. -Anterior dislocation of the hip joint: Results from a violent injury that forces the hip into extension, abduction, and lateral rotation (e.g., catching a ski tip when snow skiing). Anterior dislocation can result in injury to femoral vessels and nerves

Injury of Median nerve at the wrist

-Muscles of the thenar eminence are paralyzed and flattened -Thumb is laterally rotated and adducted -The hand looks flattened and "ape-like" -Opposition movement of the thumb is lost. -First two lumbricals are paralyzed, which can be recognized clinically when the patient is asked to make a fist , the index and middle fingers can not be flexed but the ring and little fingers can flex (Hand of Benediction) -Delicate pincer-like action of the hand is no longer possible If the median nerve is injured at the level of the wrist BEFORE it passes through the carpal tunnel many things will happen. -Thenar muscles are paralyzed (thumb movements are lost and opposition cannot be done), the thenar eminence will be flattened because of atrophy of the thenar muscles and the hand looks like a APE HAND -1st and 2nd lumbricals will be paralyzed - flexion at the metacarpal phalyngeal joint and extension of interphalyngeal joint will be lost.(so the opposite will take place)

Anterior Compartment of Arm

-Musculocutaneous Nerve (C5, C6, & C7) -Lateral Cord of Brachial Plexus 1. BICEPS BRACHII -FLEXION, but mostly SUPINATION of the forearm 2. BRACHIALIS -FLEXION the forearm *Also supplied by the RADIAL NERVE 3. CORACOBRACHIALIS -Helps in FLEXION and ADDUCTION of arm -The musculocutaneous nerve pierces the coracobrachialis then comes down to supply the biceps and the brachialis -Biceps are mainly SUPINATORS and also does flexion of the forearm HOWEVER the key flexor of the forearm is the BRACHIALIS MUSCLE!

Clinical relevance: NSAIDs & ACE inhibitors

-NSAIDs → constriction of afferent & efferent arterioles, especially in a patient with a compromised cardiac output -ACE inhibitors or angiotensin II receptor blockers →↓ Ang II actions→ relaxation of effer ent arterioles -ACE inhibitors/Ang II blockers + NSAIDs → constriction of afferent arterioles + relaxation of efferent arterioles → severe reduction in glomerular filtration rate Conclusion: combined use of NSAIDs & ACE inhibitors/AT1 receptor blockers in patients with impaired cardiac output and older patients may cause ↓ GFR and salt & water retention → ↑ blood pressure

Effective circulating volume (ECV)

-Na+ excretion depends on ECV NOT plasma [Na+] -ECV depends on blood volume & cardiac output -ECV is the pressure perfusing the vascular baroreceptors -Peripheral baroreceptors *High pressure baroreceptors **Arterial (carotid sinus & aortic arch; SNS & ADH pressure response) **Renal (juxtaglomerular cells; control renin/angiotensin/aldosterone) *Low pressure baroreceptors **Atria, large veins, pulmonary artery (control ANP) **Ventricles (control BNP)

What's the difference between osmolality & osmolarity?

-OSMOLARITY is the number of osmoles per LITER of solution -OSMOLALITY is the number of osmoles per kilogram of water/solvent -In dilute solutions, 1 liter of solution contains ~1 kg water -But 1 L of plasma only contains 0.93 L water (the rest is protein) -Suppose that 1 L plasma contains 5 milliosmoles of glucose -Then its osmolaRity is 5 mOsm/L of solution. -But those 5 milliosmoles are dissolved in only 0.93 L of water -Therefore, the glucose osmolaLity will be 5/0.93 = 5.4 mOsm/kg water -Hospital labs use a freezing point depression machine and report osmolaLity, and so shall we.

Muscles of medial/Adductor compartment of thigh Obturator nerve - ventral rami Femoral nerve - dorsal rami

-Obturator nerve (L2,3,4) 1. OBTURATOR EXTERNUS 2. ADDUCTOR BREVIS 3. ADDUCTOR LONGUS 4. ADDUCTOR MAGNUS -Has 2 parts, Adductor part and a portion of it is seen on the posterior part of the thigh called HAMSTRING PORTION, and ADDUCTOR PORTION -Has dual nerve supply. Obturator nerve for adductor portion and tibial component of sciatic nerve supplies HAMSTRING PORTION 5. GRACILES -Cutaneous innervation of obturator nerve is to the skin of medial side of thigh OBTURATOR NERVE COURSE -The obturator nerve runs along the lateral side of the pelvis, passes through the obturator foramen, and enters the thigh to innervate these muscles. *The ovaries are lying on top of the obturator nerve in the ovarian fossa. If a lady comes into the clinic and says she has spasm of the medial side of the thigh and has pain along her hip joint and knee joint it indicates that there is a problem with compression of the obturator nerve (carcinoma of the ovaries or spasm of the ovaries) -It gives one small cutaneous nerve which is innervating a patchy medial side of the skin in the thigh

Congenital hip dislocation

-Occurs in approximately 1:1000 births -Girls have higher incidence than boys -Classic signs: 1. Dislocation occurs when the femoral head is not properly located in the acetabulum. 2. Inability to abduct the thigh is characteristic of congenital dislocation. 3. In addition, the affected limb appears shorter because the dislocated femoral head is more superior to the acetabulum than on the normal side, resulting in a positive Trendelenburg sign (hip appears to drop on one side during walking). Clinical examinations: 1.Ortalani's maneuver(reduction test)-Examiner lifts and abducts the thigh and feels a "clunk" when the femoral head re-seats into the acetabulum 2.Barlow's maneuver(reverse Ortalani's)-done to discover hip instability. Baby's thigh is adducted with gentle downward pressure, dislocatable hip will be felt as head slips out of acetabulum.

Pulled elbow or nursemaid's elbow -Tear of the ANNULAR LIGAMENT could dislocate or subluxate the head of the radius out of the region

-Preschool children, particularly girls, are vulnerable to transient subluxation (incomplete temporary dislocation) of the head of the radius . -The child is suddenly lifted (jerked) by the upper limb while the forearm is pronated (e.g., lifting a child into a bus). -The sudden pulling of the upper limb tears the distal attachment of the annular ligament, where it is loosely attached to the neck of the radius. The radial head then moves distally, partially out of the annular ligament. -Treatment of the subluxation consists of supination of the child's forearm while the elbow is flexed.

Clinical aspects of sodium excretion

-Primary hyperaldosteronism (Conn's syndrome) -Adrenocortical insufficiency (Addison's disease) -Renovascular hypertension

Quadrangular Space

-Quadrangular space is just below the shoulder joint between the tedius major and tedius minor space -It is around the surgical neck area where you see the axillary nerve and posterior circumflex humeral artery -The subglenoid displacement of the head of the humerus into the quadrangular space damages the axillary nerve and posterior circumflex humeral artery

Adenosine -Cortex: Has the glomeruli, proximal and distal convoluted tubules -Medulla: Has the loop of Henle

-One of the simple ways that the blood is distributed between the blood and the medulla is via ADENOSINE -Adenosine comes from ATP -SYMPATHETIC NERVES ALSO RELEASE ATP, co-released with norepineprhine -ATP is metabolized to adenosine -In the cortex, adenosine CONSTRICTS blood vessels (Adenosine 1 Receptor) -In the medulla, adenosine DILATES blood vessels (Adenosine 2b Receptor) -When there is adenosine on board, there will be less blood flow to the cortex and more blood flow to the medulla (the blood flow is slow to the medulla and therefore we can concentrate the urine) *This is a simple redistribution of urine *When the blood vessels to the cortex are constricted, the glomeruli (which are inside of the cortex) have constricted blood vessels causing DECREASED FILTRATION PRESSURE therefore less filtrate. **If there is too much constriction in the afferent arterioles there will be decreased filtration pressure and less filtration, we compensate by allowing increased constriction in the efferent arterioles because it is POST glomerulis, causing the pressure to build up in front of it where the capillaries are *This keeps things constant so even when you're exercising you have a constant filtration rate (because if this was not constant, every time you exercise your BP would increase) -When the adenosine level goes down, the blood flow to the cortex increases and the blood flow to the medulla decreases (now we get a more diluted urine) *With low BP, we dilate the afferent arterioles and dilate the efferent arterioles

Calculation of osmolality Depends on the NUMBER OF PARTICLES

-Osmolality depends on THE NUMBER OF PARTICLES, not their size *i.e. 1 albumin (M.Wt. 67,000) = 1 Na+ (M.Wt. 23) -By weight, plasma [protein] = 7 g/dL, virtually all of dissolved solute -But protein osmolality ~ 1.5 mOsm/kg (total plasma ~285 mOsm/kg) Assuming complete dissociation: -"D5W" (5% w/v glucose) = 300 mM = 300 mOsm/kg water -150 mM NaCl = 150 mM Na+ + 150 mM Cl- = 300 mOsm/kg water -20 mM CaCl2 = 20 mM Ca++ + 2 x 20 mM Cl- = 60 mOsm/kg water

Integrity of arches of foot depends on

-Overall shape of the interlocking bones -Strength and support of pedal ligaments -Strength and tone of muscles - tibialis posterior, tibialis anterior, and fibularis longus & the Flexor Hallucis longus

Na+ reabsorption: proximal tubule THIS IS THE OVERALL STORY of whats happening int he proximal tubule -Creatinine is not reabsorbed. We look at the concentration of creatinine as we go through the proximal tubule. As we reabsorb 2/3rds of the water the creatinine concentration increases (just like calcium). So now at the end of the proximal tubule, all of the creatinine is now dissolved into 1/3 of the water (its concentration will be 3 times as high). This will continue to increase all the way through the nephron. In fact, when creatinine is excreted, by the time you get to the deep medullary collecitng duct you have reabsorbed about 99% of the water so all the creatinine is just in that 1% of water and its concentration is about 100x higher than it was in the plasma. Looking at the creatinine measure is very useful in measuring how much water is reabsorbed -Angiotensin II is released in response to a increased RENIN, which is in response to a reduced vascular volume. Here Angiotensin II increases Na reabsorption which will in turn reabsorb water, raise BP , etc.

-Overall: You have Na coming in with Tm substances (mostly in early proximal tubule). You have the Na/H countertransport system. Then you have NaCl coming into the cell via many mechanisms. This is driven by the Na/K pump THe interesting thing about this: -Proximal tubule highly permeable to H2O ::: H2O follows solute, and tubular fluid stays ~isosmotic (< 5 mOsm/kg hypotonic to plasma) *Ie. as you are reabsorbing 2/3rds of the NaCl, you're also reabsorbing water. Because you are reabsorbing NaCl and an osmotically equivalent amount of water, you are reabsorbing ISOTONIC NaCl. -ANGIOTENSIN II STIMULATES Na+/H+ countertransport system -Site of action of osmotic diuretics (urea, glucose, mannitol)

Mild sympathetic nervous activity (mechanisms)

-Partial afferent arteriole constriction →↓ GFR *Sympathetic NS (norepinephrine) directly on α1 RECEPTORS of smooth muscle → preferential constriction of afferent arteriole cells (Direct Effect) -Partial efferent arteriole constriction →↑ GFR *Sympathetic NS (norepinephrine) on β1 RECEPTORS of granular (JG) cells → ↑ renin → ↑ angiotensin II → preferential constriction of efferent arteriole cells (Indirect Effect) Partial constriction of both arterioles → unchanged GFR Both constrictions have inositol trisphosphate as second messenger

Relationship between plasma [Ca++] & [Pi] Phosphate and calcium have this close personal relationship. Calcium phosphate is not very soluble. It comes out of solution when it reaches its solubility product (calcium concentration x phosphate concentrate). If you have a solution of calcium phosphate which is saturated, then tip in phosphoric acid, you raise the phosphate level therefore calcium level will have to fall. This is because calcium phosphate is what gets precipitated. So the phosphate increases but the calcium falls. Similarly, if you ad calcium chloride you will raise the calcium level which will raise the calcium and the phosphate will fall because calcium phosphate is what gets precipitated -Calcium phosphate is deposited in bone. It does not usually get precipitated in healthy non-bone tissues because there are things like paraphosphate in those tissues which prevent the calcium phosphate. This does however happen in pathological types of tissues, calcium phosphate will get deposited and you will get precipitation. Ie. Dr. Wade has atherosclerosis in the descending aorta, so on xray you can see a calcified aorta.

-Plasma Ca++ and plasma Pi circulate at the upper limit of their solubility *i.e. at saturation: [Ca++] X [Pi] = constant (solubility product) -Therefore, if plasma [Pi] increases, plasma [Ca++] must fall, and CaHPO4 is deposited in rapidly exchanging sites in bone -CaHPO4 is not deposited in healthy non-bone tissues because of the presence of inhibitors such as pyrophosphate. -In pathological conditions (atherosclerotic plaques, scar tissue, old blood clots) CaHPO4 can be deposited (calcification)

Distribution of Renal Flow/Plasma Flow

-Plasma comes into the RENAL ARTER (100%) -Of that, 95% goes into all of the 2 million AFFERENT ARTERIOLES then through EFFERENT ARTERIOLES *Of this 90% then goes into PERITUBULAR CAPILLARIES - located around the PROXIMAL and DISTAL TUBULES in the cortex *5% goes into the VASA RECTA - located in the MEDULLA -5% goes into the PERIRENAL FAT and CAPSULE and winds up in the RENAL VEIN untouched -The pump that pumps PAH into the tubule is located in the PROXIMAL TUBULE and therefore you only pump into the tubule the PAH which went through the PERITUBULAR CAPILLARIES (the plasma that goes through the vasa recta does not get cleaned out, do not lose PAH there) -It is only the plasma that is in the PERITUBULAR CAPILLARIES that gets cleared

Tarsal tunnel

-Pneumonic: Tom Dick AN Harry -Entrapment and compression of the tibial nerve in the tarsal tunnel causes Tarsal tunnel syndrome

Calcium Balance Calcitriol drives absorption When you have a chronic high pth level (as seen in renal failure due to secondary hyperothyroidism) will lead to reabsorption, leading to osteoporosis -Deposition, reabsorption is the remodeling of the bone

-Regulated by intestinal absorption, renal excretion & bone resorption Diet (1500mg/day) -> Intestine -> Absorption (200mg/day via CALCITRIOL) + Reabsorption from caclium from the bone (500mg/day via CALCITRIOL if calcitriol is HIGH) -> Body calcium pool -> Kidneys -> Urine excretion (200mg HOWEVER this is inhibited by CALCITRIOL) PTH (CALCITRIOL) stimulates absorption of calcium in the intestine and REABSORPTION of calcium from the bone -It also helps with deposition of calcium from the body calcium pool into the bone (if calcitriol is low), and inhibits excretion of the calcitriol into the urine)

Renal Plasma Flow PAH used to find RENAL PLASMA RATE The normal range for RPF is 585-605 ml/min

-Renal blood flow (RBF) is closely related to Renal plasma flow (RPF) which is the volume of blood plasma delivered to the kidneys per unit time. -CLEARANCE tells us how much substance is cleared from the blood plasma in one minute into the urine -Clearance is the urinary concentration of any substance (Us) x the volume of urine per minute (flow of urine/V.)/Plasma concentration of any substance -Renal plasma flow could be calculated as clearance of PAH: RPF = Cs = (Us)(V.)/Ps EXAMPLE: Assume that the plasma concentration of PAH is 0.01 mg/ml, urine concentration is 5.85 mg/ml, and urine flow rate is 1 ml/min. PAH excretion (5.85 mg/ml x 1 ml/min) divided by the plasma PAH concentration (0.01 mg/ml). Thus, clearance of PAH calculates to be 585 ml/min. *PAH is used as a marker for measuring RPF because IT DOES NOT GET REABSORBED, it gets filtered and secreted *PAH is a marker that we inject IV, and now we measure the average concentration of PAH in the urine over 24 hours. Then plasma concentration of PAH is measured over several hours and average plasma concentration is documented. We then multiply Urine concentration of PAH x the flow rate of urine and divide it by the plasma concentration of PAH -If it was only filtered, we would be measuring Glomerular Filtration Rate -Filtration process is really only 20% efficient, as in only 20% gets filtered and 80% passes by the filter and goes to the efferent arterioles through the peritubular capillaries -To know the entire blood flow, you would have to have a substance that is filtered AND secreted.

In the clinic: Pedal pulse

-Routinely performed to assess the vascular supply of lower extremities -Dorsalis pedis artery is palpated lateral to Extensor hallucis longus tendon on the dorsum of foot -Vascular insufficiency results in anterior compartment syndrome -5 P signs of vascular insufficiency Pain Pallor Pulselessness Paralysis Paresthesia

Parathyroid hormone (PTH) Fall in calcium stimulates both PTH and RENIN

-Source, structure: peptide from parathyroid glands -Regulation of release: *Decreased plasma [Ca++] -> decreased calcium sensing receptor (CaSR) -> Increased PTH release Actions: 1. Increased bone resorption -> Increased plasma Ca++ & Pi 2. Increased renal 1-hydroxylase -> Increased calcitriol synthesis -> Increased intestinal Ca++ & Increased intestinal Pi absorption 3. Increased renal Ca++ reabsorption -> Decreased Ca++ excretion -> Increased plasma Ca++ 4. Decreased renal Pi reabsorption -> Increased Pi excretion -> Decreased plasma Pi Mechanism of action: Binds to a cell surface receptor -> Increased adenylate cyclase -> Increased cyclic AMP Overall effect of PTH: Increased plasma Ca++ & Decreased plasma Pi

Aldosterone actions

-Source: zona glomerulosa of adrenal cortex -Structure: steroid -Direct actions (mediated by Increased transcription & Increasedtranslation): * Increased activity of Na+ channels in principal cells of collecting duct *Increased activity of K+ channels in principal cells of collecting duct *Increased activity of Na+/K+ ATPase of principal cell -> Increase cell [K+] -> Increase K+ secretion *Increased activity of H+ ATPase of ALPHA-intercalated cells of collecting duct -Increased activity of Na+Cl- cotransporter of early distal tubule Indirect actions: -Increased Na+ uptake -> more electronegative lumen -> Increased K+ & H+ secretion

Edema: a two step process

-Step 1 *Protein-free exudate moves from the vascular bed into interstitial fluid. This movement is governed by Starling forces. -Step 2 *That reduction in vascular volume reduces blood pressure and stimulates renal retention of salt and water. *The volume of fluid retained can more than double the ~14L of interstitial fluid volume.

Mild sympathetic nervous activity *An example of mild sympathetic activity on the kidney would be as a result of MILD CARDIAC IMPAIRMENT *Because Cardiac Output is slightly reduced, mild sympathetics kicks in to keep it up at its normal level

-Stimulation of Mild sympathetic causes: Partial constriction of afferent arterioles (causing decreased glomerular capillary pressure) + Partial constriction of efferent arterioles (causing increased glomerular capillary pressure) -> Glomerular capillary pressure is unchanged -> GFR unchanged -> filtration fractures (GFR/RPF) increased -In general, the mild sympathetic nervous activity will increase vascular resistance, decrease renal blood flow, and decrease renal plasma flow leading to increased filtration fraction

Diarrhea and Hemorrhage effect on body water spaces

-Stool & blood are isotonic fluids Scenario 1: Diarrhea -> Loss of isotonic colon contents -> decreased ECF volume, ECF osmolality stays the same -> no osmotic gradient, so no net water flux -> ICF volume stays the same, ICF osmolality stays the same *↓ interstitial & ↓ plasma volume (proportionately) *causes ↑ hematocrit & ↑ plasma [protein] Scenario 2: Hemorrhage -> loss of (isotonic) blood -> decreased ECF volume, ECF osmolality stays the same -> no osmotic gradient, so no net water flux -> ECF volume stays the same, ICF osmolality stays the same *Plasma & red cells lost proportionately; no change in hematocrit.

Deltoid or Medial ligament

-Strong triangular ligament -Stabilize the ankle joint during eversion -Attachments: Above- Tip and margins of medial malleolus Below- attached to talus, calcaneus and navicular bones via four continous parts: 1. The Tibionavicular part 2. The Tibiocalcaneal part 3. Anterior and Posterior tibiotalar parts

Stability of the knee joint -The knee is not a very stable joint

-Structurally a week mechanical joint -Stability of the joint depends on: • The tone of the surrounding muscles • The ligaments that connects tibia and femur -The tone of Quadriceps femoris muscle is important in maintaining stability of the joint -Knee joint is very stable in extended position

Atrial/brain natriuretic peptide

-Structure: 28 amino acid polypeptide -Source: atrial (ANP) & ventricular (BNP) myocardial cells -Release: stimulated by Increased vascular volume -Actions: Decreased Na+ reabsorption from deep medullary collecting duct Increased GFR (afferent arteriolar dilation, efferent arteriolar constriction) Decreased renin release Decreased aldosterone release Decreased ADH release and action -Mechanism of action: Increased guanylate cyclase -> Increased cellular cyclic GMP *Note: "ANP" is family of peptides; brain NP is measured clinically

Antidiuretic hormone (ADH), a.k.a. "arginine vasopressin"

-Structure: 9 amino acid peptide -Source: supraoptic & paraventricular nuclei of hypothalamus

Brachial Plexus: Branches from the Posterior Cord MEDIAL ROTATION of the shoulder joint done by Pectorais minor , pectoralis major, teres major and subscapularis bring about medial rotation and adduction of the shoulder joint -The radial nerve is in the posterior cord, which innervates most of the extensors of the arm (extensors mostly posteriorly)

-Subscapularis & Teres major -Subscapularis innervated by UPPER and LOWER SUBSCAPULAR NERVE -Teres major innervated by JUST LOWER SUBSCAPULAR NERVE -Actions: Adduction and medial rotation of arm -Injury along the LATERAL border of Scapula - damage to the lower subscapular nerve *The nerves are traveling along the lateral border of the scapula and they go underneath the scupula to innervate these muscles. If there is injury of the scapula, it could damage the upper and lower subscapular nerves which could paralyze those muscles Axillary nerve ( C5, 6): Muscles: DELTOID and TERES MINOR Deltoid: -Anterior fibers: Flexion & medial rotation of arm -Posterior fibers: Extension & lateral rotation -Middle fibers: Abduction of arm (15-110 degree) -Teres minor: Lateral rotation of arm -Cutaneous branch: Innervates the skin over the lateral side of the arm -If there is injury to the axillary nerve, you cannot do abduction from 15-110 degrees and there may be SLIGHT rotation in doing lateral rotation (because of teres minor). Axillary nerve also innervates the shoulder skin above the deltoid muscle. If there is injury to axillary nerve, there may be anesthesia around the shoulder region.

Lymphatic drainage

-Superficial inguinal nodes: receives lymph from the thigh, perineum, gluteal region and lower abdominal wall *Horizontally placed below the inguinal ligament *Drains the entire lower limb except the LATERAL PART OF THE FOOT, and the POSTERIOR LEG -Deep inguinal nodes: receives lymph from superficial inguinal nodes and all the deep structures of the lower limb *Lies medial to the femoral vein deeper -Popliteal nodes: receives lymph from the heel, lateral side of the foot & back of the leg. -Superficial and deep inguinal nodes drain into external iliac nodes

Venous drainage

-Superficial veins: 1. Great saphenous vein -Called so because it runs the length of lower limb -Arises from the medial side of dorsal venous arch and runs ANTERIOR to the MEDIAL MALLEOUS, medially in the leg, medial to the knee, and starts running in front of the thigh and drains into the FEMORAL VEIN through the SAPHENOUS OPENING 2. Small saphenous vein -Runs behind the leg and opens up into the POPLITEAL VEIN -Deep veins: accompany the major arteries 1. ANTERIOR and POSTERIOR TIBIAL VEINS 2. POPLITEAL VEIN - anterior and posterior tibial veins join to form this 3. Popliteal vein goes on to form the FEMORAL VEIN further up in the thigh 4. Femoral vein becomes the EXTERNAL ILIAC VEIN above the inguinal ligament 5. External Iliac joins with the Internal iliac vein join to form the COMMON ILIAC VEIN 6. The two common iliac veins join to become the IVC -When a patient is having a surgery and they are immobile for a long time in the hospital, it will cause deep vein thrombosis of the lower limb. If there is a deep vein thrombosis, it will travel up through that venous path discussed above *Perforating veins: connect the superficial vein to the deep vein and drain the blood from superficial veins to deep veins, unidirectional because of the valves in the veins *Musculovenous pump - When you are walking, the muscles are contracting helping to push the blood back to the heart *Deep veins are aligned by the side of the arteries, so arterial pulsations also help push the blood back to the heart

Radio ulnar joints

-Superior and inferior radio ulnar joints: PIVOT type of synovial joint (can do rotating movements) -Middle radio ulnar joints : Syndesmosis (NO MOVEMENT INVOLVED HERE) Articular surfaces: -Superior radio ulnar joint: *Between the head of the radius, radial notch of ulna & annular ligament -Inferior radioulnar joint: *Head of ulna and the ulnar notch of radius Movements: Supination- Biceps and supinator Pronation-Pronator teres and Pronator quadratus

Sweating without fluid replacement, or diabetes insipidus

-Sweat is hypotonic (Na+ 40-60 mM, K+ 5-10 mM, Cl- 30-45 mM) -Diabetes insipidus is when the body lacks, or is insensitive to ADH Diabetes insipidus (loss of dilute urine) OR Heavy sweating without fluid replacement (loss of hypotonic saline) -> decreased ECF volume, increased ECF osmolality -> water leaves cells down osmotic gradient -> decreased ECF volume, increased ICF osmolality

Epicondylitis

-THe FLEXOR superficial muscles originate mainly by the MEDIAL EPICONDYLE -The EXTENSOR superficial muscles originate from the LATERAL EPICONDYLE -When you are using your arms too much, it will cause inflammation at the origin site, called EPICONDYLITIS GOLFER's ELBOW -Medial Epicondyle -Inflammation of COMMON FLEXOR TENDON -Affected muscles *Pronator teres *Flexor carpi radialis *Palmaris Longus *Flexor Carpi Ulnaris TENNIS ELBOW -Lateral Epicondyle -Strain attachment of COMMON EXTENSOR TENDON -Inflammation of periosteum of lateral epicondyle -Pain over lateral epicondyle and radiates down posterior aspect of forearm

Injury to the median nerve at the arm

-The median can be injured at multiple sites along its track -SUPRACONDILAR REGION - The region of the humerus that is just above the medial and lateral epicondyle -A fracture at this region can injure the MEDIAN NERVE This is also at the ANTECUBITAL FOSSA, so it can also injure the BRACHIAL ARTERY -If there is injury here, this is JUST before the median nerve gives off its branches therefore ALL of the muscle supplied by the MEDIAN NERVE and its BRANCHES will be compromised *The patient will have loss of promation (pronator teres, promator quadratus), flexion of the lateral 2 interphalyngeal joints (flexor digitorum superficialis, flexor digitorum profundus), thenar muscles will be compromised (opponuns policis-opposition of the thumb, flexor policis, and adductor policis), reduced flexion of the wrist and it will deviate medially (flexion the wrist is not completely lost because flexor carpii ulnatus, and ulnar part of flexor digitorum profoundus is still working and supplied by ulnar nerve), sensation along the lateral half of the palm is lost)

Arterial supply of the hip joint

-The FEMORAL artery is the major artery of the lower limb and is a continuation of the EXTERNAL ILIAC ARTERY -The femoral artery gives off a branch called the PROFUNDA FEMORIS ARTERY -> MEDIAL CIRCUMFLEX & LATERAL CIRCUMFLEX FEMORAL ARTERY -The medial circumflex femoral pierces the capsule and gives smaller branches which are the RETINACULAR ARTERY and supplies the head and the neck of the femur *If there is a fracture in the neck of the femur, the retinacular branches of the medial circumflex. If it continues, the head of the femur would not get any blood supply (because the other thing that used to supply the head/neck of the femur is the obturator artery but this regresses after puberty). This will cause AVASCULAR NECROSIS! •The area of the femoral head around the fovea is supplied by acetabular branch of obturator artery & medial circumflex femoral artery •The rest of the head & neck receive blood from arterial circle around the capsular ligament (medial circumflex femoral is the chief source). The retinacular arteries branches from medial circumflex femoral artery form this vascular ring, pierce the capsule & run along the neck of the femur to supply it & the head. •The arterial supply of the head & neck is solely dependent on the medial circumflex femoral artery. In the rupture of these arteries (intracapsular fracture of the neck of the femur) the head of the femur undergoes avascular necrosis.

1. Renin angiotensin aldosterone system

-The Liver secretes ANGIOTENSINOGEN & the kidney secretes RENIN -> Angiotensin I (decapeptide) -> Angiotensin II (octapeptide) triggered by ANGIOTENSIN CONVERTING ENZYME (ACE) from the lung, kidney, and vascular endothelium -> triggers the Adrenol cortex to release aldosterone

Median nerve(C5,6,7,8 &T1)

-The MEDIAN nerve is from both the LATERAL and MEDIAN CURVE -Root Value is C5, C6, C7, C8 and T1

Boundaries and Contents of the Axilla

-The PYRAMIDAL space between the UPPER THORAX and the UPPER LIMB -The APEX of the axilla is bounded by: *Anteriorly: the CLAVICLE *Medially: 1st RIB *Posteriorly: The SCAPULA -The apex of the axilla is important because there are arteries, veins and nerves traveling to the neck via the apex (it is like the gateway) The AXILLA: -Anterior boundary of the axilla: PECTORALIS MINOR and PECTORALIS MAJOR -Posterior boundary of axilla: SUBSCAPULARIS -Medial boundary of the axilla: The RIBS, and the SERRATUS ANTERIOR (muscle attached to the ribs) -Lateral Boundary of the axilla: The HUMERUS -Base of the axilla: Skin (when you lift your armpit) -There are contents in the axilla: 1. AXILLARY ARTERY 2. AXILLARY VEIN 3. BRACHIAL PLEXUS (CORDS & BRANCHES ONLY!) 4. AXILLARY LYMPH NODES -The must superficial, anterior structure in the axilla is the AXILLARY VEIN

Rotator Cuff S - Supraspinatus - Abduction 0-15 degrees I - Infraspinatus - Lateral Rotation T - Teres Minor - Lateral Rotation S - Subscapularis - Medial Rotation & Adduction

-The ROTATOR CUFF is made up of tendons from the following muscles: S - Supraspinatus I - Infraspinatus T - Teres Minor S - Subscapularis -The major contribution is the SUPRASPINATUS but SITS is the acronym that make the rotator cuff and protect the shoulder joint around it -The action of the Supraspinatus is ABDUCTION 0-15 DEGREES - Infraspinatus with Teres minor is the LATERAL ROTATION of the shoulder joint

Changes in mean arterial blood pressure

-The RPF is actually about 5x the GFR (1/5th is filtered) -The normal MEAN ARTERIAL BLOOD PRESSURE is about 90 (diastolic + 1/3 pulse pressure) -You can go beyond a BP of 90 without any significant change in renal plasma flow and glomerular filtration rate *Therefore the kidney must be increasing its resistence (partically clamping down on the afferent arterial) -parallel changes in GFR & RPF suggest afferent arteriolar constriction only -and vice versa: i.e. ↓ arterial pressure → afferent arteriole dilatation

Ulnar nerve (C8 and T1)

-The ULNAR NERVE is from the MEDIAL CORD -Root value: C8 & T1 -At the AXILLA: Does not give any branches -At the ELBOW: Does not give any branches BUT travels BEHIND the MEDIAL EPICONDYLE (funny bone) in the CUBITAL TUNNEL -At the FOREARM: As it enters, it pierces through the FLEXOR CARPI ULNARIS and gives muscular branches of FLEXOR CARPI ULNARIS, and MEDIAL HALF of FLEXOR DIGITORUM PROFUNDUS. -It also gives some cutaneous branches to the MEDIAL AXIS of the 4th digit, and supplies the DORSAL ASPECT of the MEDIAL 1 and 1/2 FINGERS -At the HAND: Does not pass through carpal tunnel, instead passes through a tunnel near carpal tunnel called GUYONS CANAL. As it enters the hand it is very closely related to the HOOK OF THE HEMETE (medial to the hook of the hemete). From here it innervates MOST of the muscles of the hand) - also called the MUSICIANS NERVE because when playing muscle instruments this is the nerve being used *Ulnar nerve innervates all the muscles of the hand except the THENAR and 1st and 2nd LUMBRICALS -Specifically, in the hand, the ulnar nerve gives a DEEP branch innervating the HYPOTHENAR MUSCLES (muscles working with the pinky finger), 3rd and 4th LUMBRICALS, PALMAR INTEROSSEI, and DORSAL INTEROSSEI

Water distribution between cellular & interstitial spaces

-The barrier is the cell membrane -Every cell contains abundant water channels (some exceptions in kidney) -Water channels consist of AQUAPORINS -Water moves passively down its concentration (osmotic) gradient therefore, all cells in body have the same osmolality (with rare exceptions)

Nephron Blood Flow

-The blood typically travels from the afferent arterioles to the efferent arterioles and then it splits *MOST of the blood will continue on to the PERITUBULAR CAPILLARIES but about 5% will go on to the VASA RECTA (in the medulla) -Then blood rejoins in the venule -The blood which supplies the vasa recta comes mostly from the JUXTA MEDULLARY NEPHRONS -Midcortical nephrons

Plain x-ray of knee joint

-The inter joint space is very important in these xrays, if it is reduced or not present it could indicate arthritis. -Lateral view of the knee taken to see the patella

Ankle joint

-Type: Synovial hinge joint -Articulation: -Above-lower end of the tibia with its medial malleolus and lateral malleolus of fibula form a mortise -Below- body/trochlea of the talus Articular surfaces are covered by hyaline cartilage

Myotatic Biceps brachii reflex

-The relaxed limb is passively SUPINATED and partially extended at the elbow. The examiner's thumb is firmly placed on the biceps tendon, and the reflex hammer is briskly tapped at the base of the nail bed of the examiner's thumb . -A normal (positive) response is an involuntary contraction of the biceps, felt as a momentarily tensed tendon, usually with a brief jerk-like flexion of the elbow. -A positive response confirms the integrity of the Musculocutaneous nerve and the C5 and C6 spinal cord segments. -Excessive, diminished, or prolonged (hung) responses may indicate central or peripheral nervous system disease or metabolic disorders (e.g., thyroid disease).

Erb's Paralysis

-The upper trunk of the brachial plexus where 6 nerves meet is called ERBS POINT -Upper trunk injury (Erb-Duchenne paralysis or Erb palsy) -Causes: Birth injury (excessive stretching of upper trunk), a violent displacement of the head from the shoulder as might result from a fall on the shoulder and during anesthesia. -Actions compromised: It results in a loss of abduction, flexion, and lateral rotation of the arm. -Deformity: WAITERS TIP HAND, In this condition, the arm hangs by the side and it is rotated medially and the forearm is pronated and extended with flexed wrist and fingers -Paralysis of muscles of shoulder and arm supplied by C5 and C6 nerves -Nerves involved : Axillary, Suprascapular and Musculocutaneous

Muscles of Anterior compartment of Forearm

-There are several muscles in the ANTERIOR compartment of the forearm -Superficial muscles 1. Pronator Teres 2. Flexor Carpi Radialis 3. Palmaris Longus 4. Flexor Carpi Ulnaris 5. Flexor Digitorum Superficialis Dogitorum - Means it is going into your 2nd, 3rd, 4th digits for its insertion Radialis and Ulnais Carpii - They are inserting at the level of carpal bones, Radialis at the lateral side, and Ulnar side at the medial side -Deep Muscles 1. Flexor Policis Longus *Polix means THUMB *This is working with the flexion of the THUMB 2. Flexor Digitorum Profondus *Again going into the fingers for its insertion and working with the fingers 3. Pronator Quadratos -The shape of the muscle is quadrangular *Action of the muscle is PRONATION -The tendon of the FLEXOR DIGITORUM SUPERFICIALIS is inserting at the MIDDLE PHALYNX of the 2nd, 3rd, 4th, and 5th fingers *Involved in flexor of the PROXIMAL PHAYLNX -The tendon of the FLEXOR DIGITORUM PROFUNDUS is inserting at the DISTAL PHALYNX *Involved in the flexor of the DISTAL PHALYNX -the LUMBRICAL muscles take their origin from the TENDON of the FLEXOR DIGITORUM PROFUNDUS

Na+ reabsorption: late proximal tubule

-There is still a Na/H cotransport system *But now there is also a countertransport system where Cl- comes into the cell and anions like FORMATE is sent out of the cell (also other anions (OH-, oxalate, SO42-) can replace formate) -The H+ and formate will combine to form FORMIC ACID (H formate). So now formate will come into the cell down its concentration gradient and it will get dissociated again and leave the cell via their consecutive cotransport systems. *The effect is, they reabsorb NaCl using the anion shuttle -ALSO, NaCl is freely going down its concentration gradients via the TIGHT JUNCTIONS

Glomerular Capillaries

-These type of capillaries are very different from muscular capillaries in that they HAVE VERY LITTLE RESISTANCE TO FLOW -The blood coming in these capillaries COME IN AT A VERY HIGH PRESSURE and VERY LITTLE FALLING PRESSURE as the blood passes through the capillaries -Relative to muscle capillaries, glomerular capillaries: • are shorter and fatter • have minimal blood pressure drop throughout length (2 in glomerular capillaries vs. 20 mm Hg in muscle) • have similar size selectivity • have about 100x permeability for water & ions • filter about 20% of plasma vs. <1%

Regulation of RBF & GFR

-They tend to be regulated similarly, some cases they are different, but typically if you regulate one you regulate the other -Afferent and efferent arterioles have smooth muscle and have the capability of constricting 1. changes in mean arterial blood pressure (autoregulation) 2. sympathetic nervous system activity mild, & severe 3. modulating effect of prostaglandins 4. atrial natriuretic peptide 5. pregnancy

Fracture of clavicle

-This can happen when you fall with an outstretched hand, or fall from a height, or difficulty baby delivery where the baby's limbs are being pulled out -The medial aspect can be pulled upwards by sternocleidomastoid -Lateral aspect can be pulled downwards by weight of upper limb -Other structures that can be involved with a clavicle fracture is the INFERIOR TRUNK of the BRACHIAL PLEXUS - (c8-T1 - making ulnar nerve) - COMPLETE CLAW HAND! HERE because all of the lumbricals are involved *Inferior trunk has anterior division and posterior division (the anterior division of the inferior trunk is making the middle part of the cord, the middle part of the cord is giving rise to the median root to the median nerve as well as the ulnar nerve) -The SUBCLAVIAN ARTERY, and SUBCLAVIAN vein can also be injured

Filtration Fraction

-Thus of the 585-605 mL of plasma that enters the glomeruli via the afferent arterioles, 125/605, or 20%, filters into Bowman's space. -The remaining 480 mL passes via the efferent arterioles into the peritubular capillaries. -This ration - GFR/RPF - is known as the FILTRATION FRACTION -Because freely filtered substances are passing into Bowman's space along with the water, about 20% of all freely filtered substances (Ie, sodium) that enter the kidney also move into Bowman's space

Branches of Brachial Plexus: From the Trunks

-Trunk: UPPER/SUPERIOR TRUNK 1. SUPRASCAPULAR NERVE *Root: C5, C6 *Muscle: SUPRASPINATUS (Initiates abduction of the arm from 0-15 degrees) & INFRASPINATUS (Lateral rotation of the arm - shoulder joint) 2. NERVE TO SUBCLAVIUS *Root: C5, C6 *Muscle: SUBCALVIUS - it is a small muscle underneath the clavicle (Steadies the clavicle)

Subtalar joint or Talocalcaneal joint

-Type: Plane synovial joint -Articulations: between the inferior surface of body of talus and middle of the upper surface of calcaneus -Movements :Inversion and Eversion of the foot -Interosseous talocalcaneal ligment helps stabilize the subtalar joint -Subtalar joint and transverse tarsal joint work together

Lunate Bone dislocation

-When this bone is fractured, it compresses the median nerve in the carpal tunnel therefore is one of the causes for carpel tunnel syndrome -When there is swelling in the synovial sheath of the tendons of the flexor nerves in the carpal tunnel (flexor digitorum profundus, flexor digitorum superficialis, flexor pollicis longus, flexor carpi radialis) then this will also compress the median nerve -Clinical features include: -Thenar muscles & 1st and 2nd lumbricals will be compromised -The patient cant do ABDUCTION, OPPSITION, or FLEXION of the thumb (opponins policis, abductor pollicis, flexor pollicis) -The patient will NOT have hand of benediction here because of flexor digitorum profundus part of it -HOWEVER, the patient will not lose sensation to the palmar lateral aspect of the hand or finger tips because the PALMAR CUTANEOUS BRANCH OF THE MEDIAN NERVE TRAVELS ABOVE the flexor retinaculum -You can do Tinnels sign - tap on the flexor retinucalum causing tingling sensation AND Funnels maneuver - flexion of the wrist 30-60 seconds and if it reproduces pain then it is positive

Hand of Benediction

-When you ask a patient to make a fist, you are asking them to flex everything -In this case, the 2nd, 3rd, and even thumb will not flex -These will not flex due to median nerve injuryIf the

Serum [creatinine] or BUN vs. GFR

-[Creatinine] & BUN ∝ 1/glomerular filtration rate -There are 3 things that affect the Urea level but with creatinine only one things affect it and thats GFR -Suppose the creatinine level is 1mg/1ml. Lets say GFR is 100ml/minute. This means that you are filtering 1ml of creatinine every minute a day (1440mg of creatinine a day being excreted). If you meausure creatinine again next semester it will still most likely be 1440mg of creatinine being excreted a day which means you are creatinine balanced (coming from the muscles). You technically are producing the exact amount of creatinine that is also being excreted per day. Now you want to donate a kidney. Now GFR goes from 100 to 50mls per minute, even though you still have 1mg/100mL of creatinine in plasma but now you are only going to filter 50ml/min or .5mg/min of creatinine. Now excretion rate has gone down to .5mg/min. Muscles don't care and they are still pumping the same. Now plasma creatinine will start to rise and it will rise until it gets to 2mL/100ml then it will stop because now at 2mg/100mL if you filter 50mL you are now back to filtering that 1mg. Because plasma concentration doubles and GFR is halfed you are now back to where you were, excreting to what you were producing.

Structure of juxtaglomerular apparatus

-all nerves in the kidney are sympathetic -granular cells = juxtaglomerular cells -

Diuresis in disease states

-not used clinically, important in disease states -diabetes mellitus Increased proximal [glucose]; renal failure Increased proximal [urea] act osmotically to Increased salt excretion & Increased water excretion -Increased proximal concentration of glucose or urea -> decreased water reabsorption -> decreased proximal Na concentration -> Decreased Na reabsorption and increased back diffusion of Na+ through tight junctions -> Increased Na excretion

Atrial (ANP) & brain (BNP) natriuretic peptide ANP - Naturally puts Na+ in the urine and causes the secretion of Na+ BNP - this is used to measure natriuretic peptide -If you expand the atrium you will increase ANP, if you expand the ventricle you will increase BNP (which is produced in the ventricle) -Ventricle expands in cases like CHF -So measuring BNP is a pretty good measure of the extent of your CHF and you can also get assays to see if your treatment is working -If you measure after treatment and BNP starts to fall, you can tell the ventricle is coming back to its regular size

-↑ blood volume → ↑ ANP (from atrium) & ↑ BNP (from ventricle) → vascular relaxation & ↑ Na+ excretion -ANP and BNP →↑ GFR & ↑RBF →↑ Na+ excretion (more actions of natriuretic peptides later) -It may or not constrict the afferent arteriole but it definitely constricts efferent arteriole -You will filter more salt and water and you will secrete more salt and water when this is present -They also cause vascular relaxation

Scapular anastomosis FIX THIS!

1. 1st part of the SUBCLAVIAN ARTERY & 3rd PART OF THE AXILLARY ARTERY -The branch of the subclavian artery anastomoses with the CIRCUMFLEX SCAPULAR BRANCH of the axillary artery 2. ANTERIOR CIRCUMFLEX HUMERAL & POSTERIOR CIRCUMFLEX HUMERAL -Brachial artery gives rise to deep brachial artery, which anastomoses with the posterior circumflex humeral. If there is a block beyond the circumflex branches, this anastomoses will work -This anastomoses is around the surgical neck 3. THORACOACROMIAL? -If there is a block before the circumflex branches, it will anastomose with thoracoacromial If there is a block, ie. because of atherosclerotic plate, it is a gradual one. The gradual block in the artery will help the collateral circulation to open up and compensate for it. If there is a sudden block, there won't be time for the collaterals to open up

Ligaments of Elbow Joint

1. Capsule 2. Ulnar Collateral Ligament -If there is a blow on the LATERAL SIDE of your arm, this could tear this ligament because it will put pressure on it 3. Radial Collateral Ligament

Use of clearance measurements

1. Clearance of inulin or creatinine measures GFR 2. Clearance of pAH is good estimate of renal plasma flow 3. Clearance of other substances explores their renal handling if Cx > Cinulin, then X is probably filtered & secreted if Cx = Cinulin, then X is probably a "glomerular substance" if Cx < Cinulin, then X is probably filtered & partially reabsorbed if Cx = 0, then X is either not filtered, or filtered & entirely reabsorbed if Cx = CpAH, then X is filtered and entirely secreted

Conents of the femoral triangle

1. Femoral nerve 2. Femoral artery 3. Femoral vein -The artery and vein are wrapped up by a sheath that is coming from the abdomen from the fascias there. Posteriorly is the fascia iliaca, and in front is the fascia transversalis -Femoral sheath is divided into 3 compartmets: 1. MEDIAL COMPARTMENT - does not have anything important other than deep inguinal lymph node *The border is called the femoral ring, and the border is called the femoral canal. Nothing there but lymph node. This is a weak area where if there is increased intraabdominal pressure, that would be a pathway for the abdominal viscera to pass through the femoral ring and femoral canal and cause femoral hernia *If femoral hernia, you would see the swelling in the FRONT OF THIGH, BELOW THE INGUINAL LIGAMENT, lateral to the pubic tubercle *Common in females *It passes through the femoral ring into the femoral canal 2. INTERMEDIATE - Femoral vein 3. LATERAL - Femoral artery *THE FEMORAL NERVE RUNS OUTSIDE OF THE SHEATH

The effect of diuretics on Ca++ excretion These are 2 important classes of diuretics Loop diuretics -> Increases Ca2+ excretion Thiazide-Like Diuretic -> Decreases Ca2+ excretion

1. Loop Diuretic -> Blocks luminal Na+K+2Cl- transporter thick ascending limb of the loop of Henle -> Increases delivery of Na+ to distal tubule -> Increases Na+ uptake by distal tubule cell -> Increases intracellular Na+ concentration -> Decreased activity of the basolateral 3Na+/Ca2+ transporter -> Decreases Ca2+ reabsorption -> Increases Ca2+ excretion 2. Thiazide-like Diuretic -> blocks luminal Na+/Cl- transporter in the early distal tubule -> decreases intracellular Na+ concentration -> Increases activity of the basolateral 3Na+/Ca2+ transporter -> Increased activity of basolateral 3Na+/Ca2+ transporter -> Increased Ca2+ reabsorption -> Decreased Ca2+ excretion

Kidney functions

1. Regulation of body fluid osmolality & volumes (hence blood pressure) 2. Regulation of electrolyte balance (Na+, K+, Pi, Ca++, Mg++, HCO3-, Cl-) *You cannot regulate ion in your body but Cl- fills in the spaces (concentration levels increase and decrease making sure you have equal numbers of cations and ions) 3. Regulation of acid base balance 4. Excretion of metabolic wastes & foreign substances (urea, uric acid, creatinine, drugs) 5. Production of hormones (renin, erythropoietin, calcitriol)

Clinical scenarios in MSK plain films

1. Trauma • Fracture • Dislocation 2. Pain without history of trauma • Fracture (stress, insufficiency, pathologic) *IE. scaphoid fracture - avascular • Arthritis • Infection • Neoplasm

Brachial Plexus: From the Posterior Cord

1. Upper subscapular (C5,6): Subscapularis - Medial rotation of arm and Adduction of arm 2. Thoraco dorsal (C6,7,8): Latissimus dorsi - Extends, adducts and medially rotates the humerus 3. Lower subscapular (C5,6): Subscapularis and teres major -Adduction and Medial rotation of arm 4. Radial: Nerve of extensor compartment of arm and forearm 5. Axillary( C5,6): Deltoid- Abduction of the arm (15-110 degree) -Teres minor-Lateral rotation of arm -Axillary nerve innervate mostly the deltoid muscle, deltoid muscle and teres minor are both innervated by the axillary nerve.

Bursitis in the knee region

1.Prepatellar bursitis/ housemaid's knee: Caused by friction between skin and patella, Seen as swelling anterior to the knee 2.Subcutaneous infrapatellar bursitis: Caused by friction between skin and tibial tuberosity, oedema occurs over the proximal end of the tibia 3.Suprapatellar bursitis: Caused by abrasions or penetrating wounds superior to patella, infection can spread to the knee joint

Fascia of the thigh *Fascia lata fuses with the PERINEAL MEMBRANE so if there is injury to the superficial pouch, the blood will not go into the leg due to the fusion of the perineal membrane with the fascia lata -The same fascia becomes FASCIA CRURA as it goes down into the leg (wrapping the muscles of the thigh tightly to hold them in place)

2 Layers: 1. Superficial fascia: contains cutaneous nerves superficial veins and lymphatics 2. Deep fascia: referred to as FASCIA LATA Invests the thigh like a strong sleeve Iliotibial tract: lateral thickened part of fascia lata, provides stability for hip and knee *Gives attachment to the Gluteus maximus and tensor fascia lata in the upper part, runs downwards and attaches to the lateral part of the knee joint *This stabilizes the knee joint in extended position (Ie. When standing still)

Skeleton of the Hand

Carpal bones: Proximal & Distal Row From Lateral to Medial (and proximal to distal) Some - Scaphoid Lovers - Lunate Try - Triquetrum Positions - Pitiform That - Trapezius They - Trapezoid Can't - Capitate Handle - Hamate

MRI- Intervertebral disc herniation

A 51-year-old man presents with pain and paresthesia along the heel of his foot. Imaging reveals an impingement of the S1 spinal nerve. Between which vertebrae does the S1 spinal nerve exit the vertebral column? S1! The patient will say they are having parasthesias of the heal portion of the foot - innervated by the TIBIAL NERVE

ABC'S of MSK plain films

A ‐ Alignment B ‐ Bones C ‐ Cartilage - Not seen in xray but seen as gaps in the joints S - Soft tissues - appear greyish in color -Water/air are black in color

Antidiuretic hormone: regulation of release

ADH release stimulated by -Increased plasma osmolality (very sensitive <1% change) via osmoreceptors in hypothalamus -Decreased blood volume (relatively insensitive >10% change) via baroreceptors in carotid sinus & aortic arch -pain, fear & other stressors (? via angiotensin II) -pregnancy -many drugs ADH release inhibited by: Decreased plasma osmolality, Increased blood volume ethanol -Increased atrial natriuretic peptide & Increased brain natriuretic peptide

AP View

ANTEROPOSTERIOR VIEW -Here you are viewing ANTERIOR STRUCTURES WELL -this is view and NOT projection (how they took the xray)

Regulation of aldosterone release

Aldosterone synthesis & release regulated by: -Increased angiotensin II plasma levels →↑ aldosterone - Increased K+ plasma levels →↑ aldosterone -↑ atrial/brain natriuretic peptide ->↓ aldosterone Also: Increased ACTH -> trophic effect on adrenal cortex

Mechanisms of H+ secretion A/Alpha intercalated cell

Alpha intercalated cell (5% of H+ secreted)

Primary aldosteronism (Conn's syndrome)

Causes: benign adenoma, benign nodular hyperplasia (idiopathic) Effects (classic trilogy): 1. hypertension 2. hypokalemia 3. metabolic alkalosis Hormonal levels: -aldosterone high (primary aldosteronism) -angiotensin II low (high bp) -renin low (high bp) At steady state (in chronic condition when balance achieved) Na+ excretion = intake; K+ excretion = intake; H+ excretion = H+ production

Angiotensin II mechanism of action

Angiotensin II -> Angiotensin receptor (AT1) -> Gq protein -> Phospholipace C -> Cleaves PIP2 -> Ip3, DAG *IP3 will go on to trigger Ca+ release from SER -> Ca-calmodulin bind to myosin light chain kinase -> Smooth muscle contraction *DAG triggers PKC (also triggered by Ca released from SER) -> Phosphorylation of target proteins

Angiotensin II actions

Angiotensin II stimulates: 1. Increased peripheral vasoconstriction -> Increased blood pressure 2. Increased aldosterone release from adrenal cortex 3.* Increased renal arteriolar constriction (efferent > afferent) 4. Increased activity of Na+/H+ countertransport in proximal tubule & thick asc. loop 5. Increased thirst & Increased ADH release * this differential effect occurs at moderate Ang II levels; at high Ang II levels both afferent and efferent arterioles are constricted

Relations of the hip joint

Anteriorly: 1. FLEXOR MUSCLES of the Hip -ILIACUS -PSOAS -PECTINEUS -Also some of SARTORIUS 2. Femoral Nerve, Femoral Artery, & Femoral Vein Posterior: 1. LATERAL ROTATOR MUSCLES of the hip -PIRIFORMIS -SUPERIOR & INFERIOR GEMELLI -OBTURATOR INTERNUS -QUADRATUS FEMORIS *These muscles all lie beneath the GLUTEUS MAXIMUS MUSCLES 2. SCIATIC NERVE (thickest nerve of the body) PosteroSuperior: 1. GLUTEAL MUSCLES Medial -ADDUCTORS & LATERAL ROTATOR MUCLES

B/Beta intercalated cell

Beta intercalated cells do the opposite of alpha intercalated cells: they secrete HCO3- into tubular fluid and reabsorb H+ into interstitial fluid they are said to proliferate in chronic alkalosis There are many more alpha intercalated cells than beta intercalated cells

Muscles of posterior compartment of the thigh

Biceps femoris -Long head-Tibial portion of Sciatic nerve -Short head-common peroneal portion of Sciatic nerve -Flexes the leg at knee joint -Extends the thigh at hip joint Semi tendinosus -Tibial portion of Sciatic nerve -Flexes the leg at knee joint -Extends the thigh at hip joint Semi membranosus -Tibial portion of Sciatic nerve -Flexes the leg at knee joint -Extends the thigh at hip joint Hamstring part of Adductor magnus -Tibial portion of Sciatic nerve -Extends the thigh at hip joint

Femoral nerve (L2,3,4)

Branches: -In the Abdomen: -Muscular branch to iliacus *Travels in front of the iliacus in the pelvis In the thigh: Divides into anterior and posterior division Anterior division 1. To Sartorius and Pectineus muscle 2. Intermediate cutaneous nerve of thigh 3. Medial cutaneous nerve of thigh Posterior division 1.Muscular branches to Rectus femoris & 3 vasti muscles 2.Saphenous nerve

Tibial nerve(L4, L5 & S1-2)

Branches: Cutaneuos branches 1. Sural nerve- supplies skin of the calf, back of the leg, Lateral border of foot and lateral side of little toe 2. Medial calcaneal nerve-supplies heel -Muscular branches- to muscles of posterior compartment of leg -Articular branches-Knee and ankle joint -Terminal branches- Medial plantar nerve *Lateral plantar nerve -Injury to tibial nerve results in paralysis of flexor muscles in the leg and intrinsic muscles in the sole of foot result in loss of plantar flexion weakened inversion of the foot thus has shuffling gait and anesthesia along the back of leg and plantar surface of the foot

Common peroneal nerve

Breaks into 2 components: -Anterior compartment (DEEP FIBULAR NERVE): 1. Tibialis Anterior 2. Extensor Hallucis Longus 3. Extensor Digitorum Longus 4. Extensor Digitorum Brevis 5. Peroneus Tertius -Inversion of foot -Dorsiflexion of Ankle joint -Lateral Compartment (SUPERFICIAL FIBULAR NERVE) 1. Peroneus longus 2. Peroneus Brevis -Eversion of foot

Primary aldosteronism (Conn's syndrome)

Case Scenario: A 38 year old man who had recorded a blood pressure of 168/96 mmHg during an insurance physical visited his family physician. His history and physical examination was unremarkable, except he had noticed that, when working out in his home gym, his regular regimen had been more exhausting than usual over the past couple of months. His blood pressure was 174/100 mm Hg sitting and standing and similar in all 4 extremities. Laboratory data: Serum: Na+ 144 mEq/L (142), K+ 2.8 mEq/L (4), Cl- 94 mEq/L (103), HCO3- 34 mEq/L (24), creatinine 1.0 mg/dl (0.6-1.2), blood urea nitrogen 16 mg/dl (7-18), glucose 88 mg/dl (fasting 70-110). Urine: Na+ 58 mEq/L, K+ 34 mEq/L, osmolality 650 mOsm/kg water. Normals in parentheses

Renovascular hypertension

Case scenario: A 32 year old woman was referred to a teaching hospital with a blood pressure of 220/120 mm Hg. Her hypertension appeared during a pregnancy, 6 years previously, and over the years has been treated with a variety of antihypertensive drugs. Blood pressure was equal in all 4 extremities, and bilateral abdominal bruits were noted on physical examination. Funduscopy showed A/V nicking, extensive hemorrhages and exudates. Her serum & urine laboratory values were within normal limits except her serum K+ 3.3 mEq/L (4). A renal arteriogram revealed bilateral fibromuscular dysplasia, with evidence of high grade obstruction on the left side.

Diabetes insipidus

Case scenario: A 38 year old man under treatment with Lithium for a bipolar mood disorder comes into your office complaining of nocturia of increasing frequency. Serum: Na+ 164 mEq/L (142), K+ 5.0 mEq/L (4), Cl- 126 mEq/L (103), HCO3- 25 mEq/L (24), creatinine 1.1 mg/dl (0.6-1.2), blood urea nitrogen 10 mg/dl (7-18). Blood pressure 116/74 mmHg lying, 88/60 standing. Urine: Na+ 2 mEq/L, osmolality 140 mOsm/kg water (50-1400). One hour after injection of 5 units of ADH his urine osmolality was 138 mOsm/kg water.

Primary (psychogenic) polydipsia

Case scenario: A 48 year old woman with a history of paranoid schizophrenia was evaluated for increasing confusion. During the examination she was quoting biblical passages and appeared fixated on some imaginary sin she had committed. Physical examination was unremarkable. Laboratory values were: Serum: Na+ 118 mEq/L (142), K+ 4.2 mEq/L (4), Cl- 78 mEq/L (103), HCO3- 25 mEq/L (25), creatinine 0.8 mg/dl (0.6-1.2), blood urea nitrogen 6 mg/dL (7-18), blood pressure 138/74 mm Hg, antidiuretic hormone undetectable. Urine: She was admitted to hospital for observation, and in the next 18 hours she produced 6.8L urine having an osmolality of 98 mOsm/kg water. One hour after treatment with nasal desmopressin and supervision to prevent water ingestion, her urine osmolarity had increased to 108 mOsm/kg. With repeated administration of desmopressin and continuing water restriction her urine osmolality reached 300 mOsm/kg over the next 6 hours.

Syndrome of Inappropriate ADH Secretion (SIADH)

Case scenario: A 56 year old woman was admitted to the hospital because of shortness of breath over the last 3 months. During the same time she had noted weight loss, hemoptysis, loss of appetite and wheezing. She admitted to being a heavy user of alcohol and cigarettes. Blood pressure 110/70 mm Hg; pulse 92/min; respiration 32/min; temperature 98.2°F. She was well developed physically but appeared pale and exhausted. Normal breath sounds were noted in the left lung but there was one area of a whistling wheeze over the upper left posterior chest. Laboratory data Serum: Na+ 110 mEq/L (142); K+ 4.5 mEq/L (4); Cl- 76 mEq/L (103); HCO3- 23 mEq/L (24); creatinine 0.8 mg/dL (0.6-1.2); BUN 12 mg/dL (7-18); total protein 8 g/dL (7); glucose 72 mg/dL (70-110); osmolality 230 mOsm/kg water (285). Urinalysis: osmolality 496 mOsm/kg water; negative for protein, glucose, ketones

Adrenocortical insufficiency (Addison's disease)

Case scenario: A 64 year old man visited his family physician complaining of fatigue, weakness, and dizziness when getting out of his bathtub. He was on a regular exercise schedule, walking 3 miles each morning and he reported that he was absolutely exhausted when he arrived home. His blood pressure was 118/72 mm Hg sitting and 80/58 mm Hg standing, pulse 122/min, temperature 97°F. His laboratory data were: Serum: Na+ 120 mEq/L (142), K+ 6.8 mEq/L (4), Cl- 90 mEq/L (103), HCO3- 18 mEq/L (24), creatinine 1.1 mg/dL (0.6-1.2); BUN 28 mg/dL (7-18); glucose 55 mg/dL (70-110). Urine: osmolality 840 mOsm/kg water (50-1200); pH 6.0; negative for protein, glucose, ketones, bacteria; a few hyaline casts. Urinary Na+ 68 mEq/L, K+ 42 mEq/L.

Adrenocortical insufficiency: causes & effects

Causes: -Degeneration of adrenal cortex (tuberculosis, autoimmune disease), & deficient ACTH Effects: -Isotonic (early disease) or hypotonic (later disease) contraction -Late disease: Increased ADH -> Increased urea reabsorption -> Increased BUN/creatinine ratio - Decreased principal cell K+ channel activity -> Decreased K+ secretion -> hyperkalemia -Decreased intercalated cell H+ ATPase -> Increased HCO3- excretion -> metabolic acidosis -Decreased glucocorticoid levels (if deficient ACTH) -> hypoglycemia

SIADH: causes & effects

Causes: lung cancer, pneumonia, many neurological conditions, many drugs Signs: hypotonic expansion (or normovolemia) inconsistency between decreased plasma osmolality & increased urine osmolality

Primary (psychogenic) polydipsia: causes & effects

Causes: psychiatric conditions Signs & symptoms: hypotonic expansion (or normovolemia) consistency between Decreased plasma & Decreased urine osmolalities often sluggish response to administered ADH (medullary "washout") patients will go to extreme lengths to drink excessive fluids Medullary washout: increased vasa recta blood flow reduced urea reabsorption from deep medullary collecting duct low ADH -> low urea permeability & high flow -> decreased [urea]

Renovascular hypertension: causes & effects

Causes: -congenital, atherosclerotic plaques, fibromuscular dysplasia Effects: isotonic expansion More affected kidney (reduced b.p.): -Increased renin release from affected kidney - Increased angiotensin II, Increased aldosterone (systemic) -> hypertension -Decreased RBF, GFR, salt & water excretion excretion by affected kidney Less affected (contralateral) kidney (increased b.p.): -Decreased RBF, GFR, salt & water excretion excretion by contralateral kidney -Increased salt & water excretion -Decreased or 0 renin secretion

Edema: decreased πc (plasma protein osmotic pressure)

Causes: Nephrotic syndrome: urinary protein loss > liver replacement (~3.5 g/day) liver disease (impaired synthesis of albumin) Nephrotic syndrome (renal protein loss >3.5g/day) OR Liver disease with decreased plasma protein synthesis -> decreased plasma protein concentration (if plasma albumin <2 g/dL) -> Increased efflux of fluid from capillaries -> generalized edema

Applied aspect: Saphenous cut down -The great saphenous vein runs superficially medial to the medial malleolus. -If a person is very dehydrated and you cannot find any veins in the upper veins, the IV can be put in the great saphenous vein locating it medial to the medial mallelous. The nerve accompyning this vein is the SAPHENOUS NERVE (Branch of the femoral nerve). It is a cutaneous nerve running with the great saphenous vein. With venous cutdown, you must be careful of this nerve or there will be anasthesias on the medial side of your leg/foot. -Great saphenous vein can also be used for coronary grafting by reversing the blood flow for CABG

Commonly great saphenous vein is often chosen for a venous cut down in an emergency (near medial malleolus), when superficial veins elsewhere are collapsed & invisible. The saphenous nerve is closely related to the Great saphenous vein in its course which is most likely to get injured during venous cut down

Transverse tarsal joint

Consists of two joints: 1.Talonavicular joint 2.Calcaneocuboid joint -Bifurcate ligament provides stability between these two joints -Movements: Inversion and Eversion of the foot

Clinical measurement of GFR using creatinine

Creatinine is produced by the body. Muscle contraction, creatine phosphate, is the piggy bank for replenishing ATP when it is used up. Creatine phosphate is metabolized to creatinine and it is an internal anhydride. Creatinine leaks out of muscles at a fairly constant rate depending on your muscle mass. If you are very muscular, you will have a larger amount of creatinine. If you have little muscle mass, you will have little creatinine. Creatinine is produced by muscle from creatine at a reasonable rate depending on your muscle mass. -Creatinine properties: 1. Produced by muscle from creatine at reasonably constant rate -Depends on your muscle mass 2. Freely filtered by kidney -Meaning the concentration in BOWMANs space is exactly the same as it's concentration in the PLASMA -It goes through that filtration barrier just as easily as water does 3. Not reabsorbed 4. Slightly secreted (~10% of excreted creatinine is secreted) 5. Hence: GFR (close approximation) = Ccreat = Ucreat x V/Pcreat -So you get a little bit more creatinine in the urine than was filtered -The clearance (the volume which supplies the amount of creatinine that was secreted) is a little more than the volume thats filtered, taken from the peritubular capillaries. So you get creatinine from a little bit more plasma than what was filtered -So the volume cleared is the volume filtered + 10% more from that little bit of creatinine that was secreted -

Relations of the Elbow Joint

Cubital fossa: Boundaries: Medially-PRONATOR TERES Laterally- BRACHIORADIALIS Superiorly - line connecting the epicondyles Roof- deep fascia and medial cubital vein *Median CUBITAL VEIN - connects the BASILIC VEIN on medial side and CEPHALIC VEIN on the lateral side *This is the most common vein used for IV punctures to draw blood *A catheter can also be passed through the medial cubital vein to go through the basilic vein to reach the axillary vein Contents:(from medial to lateral) Median nerve Brachial artery Tendon of Biceps brachii muscle Bicipital aponeurosis

The macula densa and renin secretion

Decreased arterial blood pressure -> decreased glomerular filtration rate -> decreased Na+ & Cl- to macula densa -> Decreased Na+ & Cl- uptake by macula densa cells -> Decreased ATP release and Decreased adenosine release -> Decreased binding to their receptors on the extraglomerular masangial cells, P2 and A1 respectively -> Decreased intracellular calcium concentration leading to decreased intracellular calcium concentration in the juxtaglomerular cells, masangial cells and afferent arteriole smooth muscles all connected to each other by gap junctions -> Increased renin (specifically released by juxtaglomerular cells) -> vasodilateion -> Tubuloglomerular feedback -> Increased GFR

Clinical aspects of water excretion

Diabetes insipidus nephrogenic, neurogenic (central) Syndrome of inappropriate ADH secretion (SIADH) Primary (psychogenic) polydipsia

Body calcium Virtually all calcium is in the bones but the calcium that is not in your bone is very important (either extracellular or in your SER).

Distribution: ~99% in bone, as calcium hydroxyapatite Plasma [Ca++]: *10 mg/dL (used clinically), 2.5 mM, 5 mEq/L *50% ionized, 10% complexed to citrate/phosphate, 40% protein bound i.e. only 60% of plasma [Ca++] filtered Protein (serum albumin) binding: -H+ occupies calcium binding sites on the albumin. If your H+ increases then H+ will muscle the calcium off of those binding sites and the free calcium will increase. Paradoxically, if calcium increases then contractility of the muscle cells decreases *Increased [H+] (decreased pH) -> Increased ionized Ca++ -> arrhythmias, decreased neuromuscular excitability *Decreased [H+] (Increased pH) -> Decreased ionized Ca++ -> hypocalcemic tetany Regulatory hormones: *parathyroid hormone (PTH) from parathyroid gland *vitamin D3: activated by liver & kidney -> 1,25(OH)2D3 (calcitriol) *calcitonin: from parafollicular cells of thyroid, stimulates bone formation, not important in humans, salmon calcitonin pharmacology

Tm-dependent reabsorption mechanisms Tm = Transport maximum

Examples: glucose, galactose amino acids organic acids (acetoacetate, b hydroxybutyrate, lactate, etc.) *phosphate, *sulfate vitamin C *phosphate reabsorption: regulated by parathyroid hormone (only a very small amount of phosphate gets excreted) *sulfate reabsorption: regulated by kidney; not physiologically important (only a very small amount of phosphate gets excreted) For all other transport maximum substances: kidney excretes excessive plasma concentrations, but is not the normal regulator of their body concentrations.

Determination of Tm glucose -Initially, the rate reabsorbed is the rate filtered -At Tm, every glucose transporter on all proximal tubules of the kidneys are moving at their maximum rate.

Experimental procedure: -give IV infusion of inulin & progressively increasing [glucose] *Inulin given to measure GFR *Started off with no glucose, and consecutively increased glucose every 30 minutes, checking urine every 30 minutes *Trying to measure the maximum rate that the kidneys can reabsorb glucose -collect urine over timed clearance periods -take blood sample at mid time of each clearance period *Trying to measure the maximum rate that the kidneys can reabsorb glucose Measure: -glomerular filtration rate (Cin); units: ml/min -filtered load of glucose (GFR x Pglu); units: mg/min -excretion rate of glucose (Uglu x V); units: mg/min Calculate: -glucose reabsorbed (glucose filtered - glucose excreted)

Daily H+ production

Fixed acids (all except H2CO3): source: oxidation of S- & P-containing proteins & some aminoacids quantity: ~ 70 mEq/day excreted by kidney Volatile acids (H2CO3): source: oxidation of C-containing nutrients quantity: ~ 13,000 mEq/day excreted by lung

Movements of the hip joint

Flexion Iliopsoas, Rectus femoris and Sartorius and also by adductor muscles Extension Gluteus maximus and the hamstring (muscles of posterior compartment of thigh) muscles Abduction Gluteus medius, Gluteus minimus and assisted by Sartorius, Tensor fascia latae and piriformis Adduction Adductor longus, Adductor brevis, adductor fibers of Adductor magnus and assisted by Pectineus and Gracilis Lateral rotation Piriformis, Obturator internus and externus, Superior and inferior gemelli and Quadratus femoris, assisted by Gluteus maximus Medial rotation Anterior fibers of Gluteus medius, Gluteus minimus and Tensor fasciae latae

Movements

Flexion •Hamstrings •Sartorious •Gracilis •Popliteus initiates the flexion Extension •Quadriceps femoris Medial Rotation •Sartorius •Gracilis •Semitendinos us Lateral Rotation •Biceps femoris

Femoral Triangle

Found just below the inguinal ligament in the upper 1/3 part of the thigh Boundaries: -Superior - Inguinal Ligament -Medially - Adductor Longus -Laterally - Sartereous -Roof - Skin and fascia -Floor - Some muscles, PSOAS, PECTINEUS, ADDUCTOR BREVIS

Bennett's Fracture Dislocation

Fracture at the lower end of the 1st metacarpal -Also sesamoid bones at the 1st MPC joints can often be confused as a fracture fragment but they are not! they are normal

Injury to Common peroneal nerve

Fracture of fibular neck may cause injury to common peroneal nerve, which winds around the neck of fibula. This results in paralysis of muscles of anterior and lateral compartments of leg (dorsiflexes and evertors of the foot),causing Foot drop, high stepping gait and anesthesia on the dorsum of the foot

Contents of Popliteal fossa

From lateral to medial: 1. Common fibular nerve of Sciatic Nerve *Almost completely running laterally 2. Tibial Nerve of Sciatic Nerve 3. Popliteal Vein *Around this is the popoliteal group of lymph nodes 4. Popliteal artery

Tm-dependent features

General properties: 1. freely filtered, i.e. [Bowman's capsule] = [glomerular plasma] - goes through filtration in bowmans space just like water would (so its concentration in Bowmans Capsule = its concentration in the Plasma) 2. reabsorbed from PROXIMAL TUBULE -This is where the pumps are 3. transported at the luminal (apical membrane) membrane by Na+ linked cotransport (symport) *i.e. secondary active transport 4. transported at the basolateral surface by variety of mechanisms *e.g. glucose: facilitated diffusion (passive, carrier mediated) *e.g. ketoacids, phosphate, amino acids (various mechanisms) 5. transport at the luminal membrane shows saturation

Countercurrent Multiplier

Generation of the medullary osmotic gradient (NaCl & urea) active, energy provided by thick ascending limb -Na+/K+ATPase pump -urea accumulation passive, secondary to NaCl gradient *The reabsorption of Na in the absence of water driven by the Na/K pump in the thick ascending imb

Plain X-ray Elbow joint

Head of the radius is also articulating with the ulnar - called the SUPERIOR RADIOULNAR JOINT being held together by the ANULAR LIGAMENT

Creatinine & Blood Urea Nitrogen (summary) Note: these values are just examples *Reliability of methods for determining GFR: check creatinine clearance > check serum [creatinine] > check BUN

Healthy Subject: -Creatinine (mg/dL): 1 -BUN (mg/dL): 15 -BUN/Creatinine ratio: 15 Renal Failure (25% GFR): -Creatinine (mg/dL): 4 -BUN (mg/dL): 60 -BUN/Creatinine ratio: 15 Dehydration Subject: -Creatinine (mg/dL): 1.5 -BUN (mg/dL): 45 -BUN/Creatinine ratio: 30 Renal Failure (25% GFR) & dehydrated: -Creatinine (mg/dL): 6 -BUN (mg/dL): 180 -BUN/Creatinine ratio: 30

Plain radiographs of lower limb Hip joint (AP view)

Here you must see Shenten's line

Regulation of K+ excretion

Homeostatic regulation of body K+ dietary K+ aldosterone collecting duct fluid flow Pathological states acid base conditions diuretic use

Why does Na+ excretion fall back to equal to Na+ intake?

Hydrochlorothiazide (HCTZ) →↓ distal NaCl transporter →↑ Na+ excretion ↓ vascular volume →↑ RAA system, →↑ SNS, →↓ ANP/BNP, ↓ GFR ↑ Aldosterone →↑ Na+ channels in collecting duct principal cell ↑ Angiotensin II →↑ Na+/H+ transporter in proximal & ascending loop ↓ natriuretic peptides →↑ Na+ reabsorption in medullary collecting duct ↓ GFR (modulated by autoregulation) →↓ Na+ filtered →↓ Na+ excreted All the above act at different sites from HCTZ to reduce Na+ excretion and return the subject to Na+ balance

Regulation: K+ depletion -> Increased H+ secretion

Hypokalemia has only a weak stimulatory effect on H+ secretion But Decreased [K+] and Increased aldosterone together powerfully stimulate H+ secretion

Fracture neck of Femur are of 2 types - Intracapsular fracture of femoral neck or hip dislocations tear medial circumflex femoral artery which result in avascular necrosis of femoral head - In intracapsular fracture, the affected limb is shortened and held in characteristic laterally rotated position with toes pointing laterally. - Extracapsular fracture of neck (eg.inter-trochanteric fracture), the retinacular arteries are saved, hence healing is faster

INTRACAPSULAR FRACRURE - Medial circumflex artery would be compromised leading to AVASCULAR NECROSIS EXTRACAPSULAR FRACTURE (INTROCHANTER FRACTURE) - The medial circumflex - retinacular branches are not involved and the head/neck of the femur would still receive its blood supply

Sodium balance (diuretic)

If you have monozygotic twins and they are on the same diet, but you treat only one with a diuretic like HTCZ. This will cause that twin to secrete salt and water and their body mass will be decreased. However after a couple of weeks, they bot will be excreting the same amount of salt and water (because the body does not make salt) -Subject is treated with hydrochlorothiazide (HCT) from day 5 -Net Na+ loss (days 6-13) = 240 mEq = ~1.8 L from extracellular space

Myogenic Control of Afferent Ateriole Tone *Purely muscle response

Increased MAP -> Increased stretch of afferent arterioles -> Opening of mechanically gate Na+ & K+ channels in smooth muscle -> becasue cell is negative, Na+ influx > K+ efflux -> Muscle cell depolarizes (ie less negative) -> Opening of voltage gated Ca++ channels -> Ca++ enters cell, binds to calmodulin, activates MLCK, muscle contracts

Regulation: Increased angiotensin II -> Increased H+ secretion

Increased Na+/H+ exchanger (proximal tubule/thick ascending limb) -> Increased H+ secretion

Regulation: Increased PaCO2 -> Increased H+ secretion

Increased P.CO2 -> Increased H+ synthesis (mass action) -> Increased H+ secretion (metabolic compensation for respiratory acid-base defects

Tubuloglomerular Feedback on Afferent Arteriole Tone -In these cells ADENOSINE stimulates the contraction of smooth muscle cells indirectly -In the coronary circulation of the heart, it is a vasodilator and relaxes it, increases blood flow to the coronary circulation of the heart

Increased arterial blood pressure -> Increased glomerular filtration rate -> Increased Na+ & Cl- to Macula Densa -> Increased Na+ & Cl- uptake by macula densa cells -> Increased ATP release (P2 receptor) AND Increased Adenosine Release (A1 receptor) -> Extraglomerular Masangial Cells (will have increased intracellular Ca++), these are connected to -> Masangial cells via GAP Junctions (causing increased intracellular Ca++), also connected to Juxtaglomerular cells (which has increased intracellular Ca++ leading to decreased renin release), and afferent arteriole smooth muscle (which has increased intracellular Ca++ *Both masangial cells and afferent arteriole smooth muscle cause vasoconstriction leading to tubuloglomerular feedback -> DECREASED GLOMERULAR FILTRATION RATE -more about renin release later -note: contrast the effect of adenosine on coronary arterioles

Regulation: Decreased pH -> Increased H+ secretion

Increased extracellular [H+] (decreased pH) -> Increased H+ entry into tubular cells ->Increased H+ secretion Mechanisms: 1. mass action effect of Increased intracellular [H+] 2. Decreased pH -> allosteric stimulation of Na+/H+ transporter 3. acute acidosis causes movement of Na+/H+, HCO3-/Cl-, 3HCO3-/Cl-, and H+ ATPase transporters into cell membranes where they are active (4. alkalosis causes movement of Na+/H+, HCO3-/Cl-, 3HCO3-/Cl-, and H+ ATPase transporters into intracellular vesicles where they are inactive)

Intake & output of sodium Sweat is actually a HYPOTONIC SOLUTION. The sodium concentration is LESS than the concentration of water/plasma. If you sweat and do not replace the fluid, the volume will fall but the osmolality will increase because you are losing more water than you are salt.

Intake: -most dietary Na+ is added during food preparation -daily intake ~150 mEq/day (low salt diet <50 mEq/day) Output: -renal excretion: regulated -sweating: sweat is hypotonic ([Na+] 30-65 mEq/L) -> hypertonic contraction Plasma [Na+]: -138-145 mEq/L; serum osmolality ~ 2 x [Na+] Urinary [Na+]: -range 5-200 mEq/L; depends on intake, urine volume, and renal function

Recap on INULIN

Inulin is filtered. Once filtered it is neither reabsorbed, nor secreted, nor metabolized, nor synthesized by the kidney. Once it crosses the filtration barrier it is history (out in the urine) -The weight of inulin that is filtered is the glomerular filtration rate x the plasma inulin concentration *WEIGHT OF INULIN which is FILTERED = GRF x concentration of inulin in plasma (volume x concentration gives a weight) *INULIN EXCRETED = Urine flow x Urine concentration (volume x concentration = weight) -Because of the way the kidney handles inulin specifically (and similar substances), we can say that the inulin filtered = the urine flow x urine inulin *GFR = Weight excreted divided by the plasma inulin -Clearance is the volume of plasma which supplies the weight of a substance that is secreted (in the case of inulin it is the volume that is filtered, and here all that is filtered and secreted) If you double the concentration of plasma inulin then you will double the inulin excreted and they will cancel out and your clearance will not change

K+ handling by the kidney

K+ excretion depends on the rate of K+ secretion by principal cells

K+ secretion by principal cell

K+ secretion depends on: electrochemical gradient (cell tubular fluid) K+ channel activity

Regulation of H+ secretion: K+ sparing diuretics

K+ sparing diuretics inhibit H+ secretion & excretion

Pathological conditions: K+ sparing diuretics

K+ sparing diuretics inhibit K+ secretion & excretion reminder! K+ sparing diuretics block Na+ channels, not K+ channels

Nephron segments

Key (learn these): -Bowman's capsule -Proximal tubule -Thin descending limb (loop of Henle) -Thin ascending limb (loop of Henle) -Thick ascending limb (loop of Henle) -Macula densa -Distal convoluted tubule -Connecting tubule -Cortical collecting duct -Outer medullary collecting duct -Deep medullary collecting duct In the human kidney: 85% superficial/mid-cortical nephrons 15% juxtamedullary nephrons

Injury to the Musculocutaneous Nerve

Leads to: 1. Loss of sensation on the lateral surface of the forearm 2. Paralysis to the CORACOBRACHIALIS & BICPES BRACHII which leads to WEAKENED FLEXION and SUPINATION of the forearm

Mesangial cells

Location -Most are tucked around the bases of the glomerular capillaries -Some are extraglomerular lying between the afferent & efferent arterioles and the macula densa cells of the thick ascending limb. See "juxtaglomerular apparatus" later Functions -Contain actin and can contract, squeezing the glomerular capillaries and affecting blood flow & glomerular filtration -Secrete an extracellular matrix. -Have phagocytic properties and can remove unwanted macromolecules. -Secrete prostaglandins cytokines and other paracrines

Anterior Compartment (FLEXOR) of Forearm

MEDIAN NERVE: 1. Pronator Teres - Pronation & Flexion of Forearm 2. Flexor Carpi Radialis - Flexion and Abduction of Hand 3. Palmaris Longus - Flexion of hand 4. Flexor Digitorum Superficialis - Flexion of proximal interphalangeal joints of medial four digits ANTERIOR INTEROSSEOUS NERVE 1. Flexor Digitorum Profundus 2. Flexor Pollicis Longus - Flexion thumb phalanges 3. Pronator Quadratus - Pronation of forearm -Anterior Interosseous nerve is a branch of the MEDIAN NERVE ULNAR NERVE 1. Flexor Carpi Ulnaris - Flexion and adduction of hand 2. Flexor Digitorum Profundus - Flexion of digital interphalangeal joints of medial four digits *Flexor digitorum profundus of the INDEX and the MIDDLE FINGER - MEDIAN NERVE (Therefore if you are flexing the distal phalynx of the index and the middle finger you are testing for the medial nerve) -Flexor digitorum profundus of the RING FINGER and PINKY FINGER - ULNAR NERVE (Therefore if you are flexing the distal phalynx of the ring finger and pinky finger you are testing for the ulnar nerve)

Femoral artery Femoral pulses - you go below the inguinal ligament, midpoint. Palpate the artery against the head of the humerus -When you want to anesthesize the femoral nerve, you find the pulses of the femoral artery, go laterally you have the femoral nerve where you can place the anesthesia

Major artery of lower limb Branches: 1.Profunda(deep) femoris artery -Medial & lateral circumflex branches -2 to 3 perforating branches (closely related to the shaft of the femur) *Fracture at the shaft of the femur will injure the perforating branches of the perfounda femoris and cause hematoma at the back of the thigh 2.Supeficial circumflex iliac 3.Superficial epigastric 4.Superficial & Deep external pudendal 5.Deep genicular artery -Continuation of femoral artery- Popliteal artery *After the femoral artery passes in the femoral triangle adductor canal, it will go into the adductor hiatus and enter the back of the knee as the popliteal artery

Why do clinicians care about the body's pH

Many clinical conditions result in characteristic changes in body pH. Defining the particular acid base condition helps in the differential diagnosis of some diseases.

Anastomosis around the elbow joint

Medial Side 1. Superior Ulnar Collateral with Posterior Ulnar Recurrent 2. Inferior Ulnar Collateral with Anterior Ulnar Recurrent Lateral Side 1. Radial Collateral (Anterior Descending) with Radial Recurrent 2. Middle Collateral (Posterior descending) with Interosseus Recurrent -Prevents ischemia in the forearm region

Gluteal region

Muscles of the Gluteal region 1. Gluteus Maximus UNDERNEATH GLUTEUS MAXIMUS 2. Gluteus Medius (towards posterior superior side) 3. Gluteus Minimus - below gluteus medius 4. PIRIFORMIS is underneath the gluteus maximus and just below the gluteus medius 5. Below piriformis is the SUPERIOR AND INFERIOR GEMELLI 6. Between the gemeli is the oburators internus and externus 7. The lower most part of the gluteal region is the quadrangular muscle, quadratos femoris LATERAL ROTATORS: 1. Piriformis 2. Obturator Internus 3. Obturator Externus 4. Superior Gemeli 5. Inferior Gemeli 6. Some help from QUADRATOS FEMORIS

Ammonia synthesis by the kidney

NH4+ excretion NH4+ secretion by Na+/H+ countertransport in proximal tubule some NH4+ reabsorption in thick ascending limb of loop of Henle NH3 trapping (as NH4+) as tubular fluid acidified in collecting duct

NaCl & H2O excretion with volume expansion

NaCl & water excretion is increased by the following mechanisms 1. Decreased sympathetic nervous activity (Increased Na+ excretion) 2. Increased ANP & BNP release from the heart (Increased Na+ excretion) 3. Decreased ADH (Increased H2O excretion and Increased Na+ excretion) 4. Decreased renin secretion (via Decreased angiotensin II, decreased aldosterone) 5. Decreased angiotensin II (Increased Na+ excretion) 6. Decreased aldosterone (Increased Na+ excretion) 7. Increased GFR (modulated by autoregulation) -> Increased Na+ excretion and vice versa for volume contraction all the Increased arrows are Decreased, & Decreased arrows are Increased

Diabetes insipidus: causes & effects

Neurogenic (central) diabetes insipidus (lack of ADH secretion) Causes: idiopathic, neurosurgery, trauma, primary or secondary malignancy Nephrogenic diabetes insipidus (renal insensitivity to ADH) Causes: lithium toxicity, hypercalcemia, osmotic diuresis (diabetes, acute or chronic renal failure), congenital (rare) Neurogenic vs. nephrogenic diabetes insipidus: give ADH (or desmopressin) if urine osmolality increased then neurogenic DI if urine osmolality unchanged then nephrogenic DI Signs & symptoms of diabetes insipidus: Hypertonic contraction Excessive urination & thirst Hypernatremia (usually limited by thirst mechanism) Inconsistency between Increased plasma osmolality & decreased urine osmolality

New HCO3- added to the body in various states

New HCO3- = titratable acidity + urinary NH4+ + urinary HCO3-

Regulation of K+ distribution

Normally, 98% of total body K+ is intracellular

Autoregulation: key points

Note: autoregulation does not reduce GFR; it minimizes the increase caused by increased blood pressure Autoregulation: ↑ b.p. → ↑ afferent arteriole resistance → minimal ↑ GFR 1. disappears when mean arterial pressure < 85 mm Hg sympathetic activity overrides afferent arteriole relaxation 2. not perfect ↑ blood pressure → small but important ↑ GFR can be over-ridden by hormonal & nervous influences

Obturatory Nerve - Applied Anatomy

Obturator nerve: -Referred pain:- In diseases of hip joint- pain on the medial side of the thigh or the knee jt. along the obturator nerve - since the nerve supplies both joints. -Inflammation or carcinoma of ovary:- peritonitis affect the ovarian fossa - irritation of obturator nerve - referred pain to the hip, knee and inner side of the thigh and spasm of adductor muscles.

Pathological conditions: loop & thiazide diuretics

Overview: loop & thiazide (L&Ts) diuretics stimulate K+ secretion & excretion Mechanisms: 1. L&Ts →↓ vascular volume →↑ renin, angiotensin II, aldosterone aldosterone →↑ K+ secretion & excretion 2. L&Ts →↑ Na+ delivery to principal cell →↑ Na+ reabsorption ↑ Na+ reabsorption →↑ K+ secretion & excretion 3. L&Ts →↑ collecting duct flow →↑ K+ secretion & excretion

Sodium excretion

Overview: -Na+ is freely filtered , ~99.5% is reabsorbed, 0.5% excreted -The ~0.5% excreted is called the fractional excretion of Na+ (FENa+) Sites of reabsorption: -65% from proximal tubule -25% from thick ascending limb of loop of Henle -5% from distal tubule -3-5% from collecting duct (most important site of regulation)

Interossei Muscles

PALMAR INTEROSSEI MUSCLES -Ulnar nerve -Adduction of fingers DORSAL INTEROSSEI MUSCLES -Ulnar nerve -Abduction of fingers Adduction and abduction of the fingers are both done by the ULNAR NERVE -To test the ulnar nerve here, you: 1. Place a paper in between the patients fingers and ask them to hold it tightly, testing adduction (Palmar Interossei) 2. Ask the patient to spread out the fingers, testing abduction (Dorsal interrossei)

Pharmacological diuretic actions: general mechanism

Pharmacological diuretic -> Decreased Na+ reabsorption -> Increased Na+ excretion -> Decreased plasma Na+ concentration -> Decreased plasma osmolality PRIMARY ACTION: -Pharmacological diuretic -> Decreased Na+ reabsorption -> Increased Na+ excretion (which leads to isotonic extracellular volume contraction leading to decreased edema or decreased hypertension) -> Decreased plasma Na+ concentration -> Deacreased plasma osmolality (which can lead into the secondary action) SECONDARY ACTION: -Decreased plasma osmolarity -> Decreased ADH concentration -> Decreased water reabsorption -> Increased water excretion -> Isotonic extracellular volume contraction -> Decreased edema or decreased hypertension

Take home points

Plain films are the workhorse of MSK radiology • Combining the clinical scenario with the ABC's can help guide you to the correct diagnosis • If trauma, is there a fracture or misalignment? • If pain with no trauma, consider arthritis, tumor, infection, tendon pathology

Important principles 2

Plasma [HCO3-] depends on the rate of renal H+ secretion Increased H+ secretion -> Increased plasma [HCO3-] (metabolic alkalosis) Decreased H+ secretion -> Decreased plasma [HCO3-] (metabolic acidosis) Healthy kidney maintains the constancy of plasma [HCO3-] by maintaining constancy of H+ secretion (irrespective of moderate acid or alkaline assaults)

Renal phosphate handling

Plasma [phosphate]: -~15% protein-bound, therefore ~85% is freely filtered Phosphate reabsorption: -on normal diet: ~80% reabsorbed, ~20% excreted -reabsorption sites: ~90% proximal (Tm mechanism), <10% distal Regulation of phosphate excretion: -Pi filtered load slightly greater than reabsorptive capacity *kidney regulates plasma [Pi] -An increase in GFR -> Increased filtered load Pi -> Increased Pi excretion Parathyroid hormone (PTH) -PTH -> Increased proximal Pi reabsorption -> Increased Pi excretion Note: at physiological pH's phosphate is a mixture of H2PO4- and HPO42-, hence the use of the symbol Pi.

Tibial nerve

Posterior compartment breaks into 2 -Superficial Muscles: 1. Gastronemius 2. Soleus 3. Plantaris -Plantar flexion at ankle joint -Deep Muscle 1.Popliteus------unlocks the knee joint 2.Flexor digitorum longus----Flexes distal phalanges of the lateral four toes 3.Flexor hallucis longus-----Flexes distal phalanx of big toe 4.Tibialis posterior-----Inversion of foot at subtalar joint

In the clinic: Palpation of posterior tibial artery

Posterior tibial artery is palpated between the medial malleolus and the calcaneal tendon

Countercurrent Exchanger

Preservation of the medullary osmotic gradient passive, water & solute exchange by vasa recta -occurs in vasa recta (capillaries)

Measurement of GFR using inulin INULIN FILTERED = INULIN EXCRETED The weight of the inulin filtered is the VOLUME that is filtered x the concentration of inulin in that filtrate -If Inulin is filtered, not reabsorbed and not secreted, then the inulin filtered = inulin excreted. So shouldn't the plasma inulin concentration = urine inulin concentration? No! Because as you filter, as you go through the nephron, you reabsorb water so the inulin in the filtrate gets more and more and more concentrated. Typically the GFR in human is 120mL/minute. If you multiply that by the number of minutes a day, you wound up with about 180L of fluid, but typically a day you produce ~1.5L of urine (only about 1mL excreted per minute). The inulin that was originally in the 120mL that was filtered, winds up being 1mL, so its concentration is going to be much higher since water is being taken from the urine filtrate. GFR for inulin = Clearance of inulin

Properties of Inulin -Polyfructose, M.Wt. 5000 -Freely filtered i.e. [Bowman's space] = [plasma] -Not reabsorbed -Not secreted -Not metabolized or synthesized -Therefore: inulin filtered = inulin excreted -inulin filtered (mg/min) = GFR (ml/min) x Pinulin (mg/ml) -inulin excreted (mg/min) = urine flow (ml/min) x Uinulin (mg/ml) therefore: -GFR x Pinulin = urine flow x Uinulin or: GFR = Uinulin x urine flow/ Pinuline = Uin x V./Pin 1. Give an intravenous infusion of inulin 2. Allow time for equilibration (constant plasma [inulin]) 3. Collect urine over specified clearance period (e.g. 2 hours) 4. At mid point of clearance period, take a blood sample 5. Measure V, Uinulin, & Pinulin 6. Calculate: Cinulin = Uinulin x V (= GFR)/Pinulin -The Cinulin is independent of Pinulin concentration because: -if Pinulin is doubled then Uinulin will be doubled and Cinulin is unchanged (clearance will not change)

Why does the body care about its pH?

Proteins bind H+ reversibly. If the [H+] in the environment of proteins changes, they will gain or lose H+. This alteration in charge configuration changes the shape, and therefore the function, of proteins. Enzymes, regulators, muscles, & transporters are all proteins.

H+ secretion (proximal tubule & thick ascending limb)

Proximal tubule (80%), thick ascending limb (15%) of H+ secreted

Renovascular hypertension: causes & effects

SEE RENAL PAPER NOTES

Pain without trauma: Osteoarthritis of knee

Reduced joint space

Vitamin D3 & calcitriol (1,25 dihydroxycholecalciferol) -Osteoblast deposits and remodels bone, and also facilitates the affect of PTH on calcium reabsorption from the distal tubule -Osteoclast breaks down bone

Regulation of plasma [calcitriol]: -Increased PTH -> Increased renal 1-hydroxylase -> Increased calcitriol -Sunlight & dietary sources -> Increased vitamin D3 -> Increased calcitriol Actions of calcitriol: 1. Increased Ca++ & Pi absorption from intestine (PTH facilitates) 2. Facilitates PTH -> Increased bone resorption & Increased osteoclast activity (remodels) 3. Facilitates PTH -> Increased Ca++ reabsorption from distal tubule

Renal failure and secondary hyperparathyroidism Renal failure is reduction of GFR -If you have chronic kidney failure and you find someone to give a kidney transplant, the first thing they do is cut out 3/4ths of your parathyroid gland because it'll be hypertrophied. Once you have a normal GFR you will then have hyperparathyroidism

Renal failure -> Decreased glomerular filtration rate -> Decreased phosphate filtered -> Decreased phosphate excreted -> increased plasma phosphate concentration -> decreased calcium concentration -> Increased parathyroid hormone secretion & parathyroid hypertrophy -> secondary hyperthyroidism

Regulation of renin release

Renin release is stimulated by: 1. Decreased blood pressure in afferent arteriole (direct effect on juxtaglomerular cells) 2. Decreased Na+ & Cl- delivery to macula densa (Decreased ATP/adenosine -> Decreased smooth muscle [Ca2+] -> Decreased jg cell [Ca2+]) 3. Increased sympathetic activity (BETA 1 adrenergic receptors on juxtaglomerular cells) 4.Decreased atrial natriuretic peptide -> Increased renin release

Unhappy triad

Results due to lateral blow to the flexed knee -Medial meniscal tear -Rupture of tibial/medial collateral ligament - Rupture of anterior cruciate ligament

Rotator Cuff Muscles

S- Supraspinatus I- Infraspinatus T- Teres Minor *All three of these at the GREATER TUBERCLE of the humerus *Involved in LATERAL ROTATION of the arm S- Subscapularis *At the LESSER TUBERCLE of the humerus *Involved in MEDIAL ROTATION & ADDUCTION of the arm

Adrenocortical insufficiency: flow charts At steady state (balance): -normal Na+ excretion, normal K+ excretion, normal H+ excretion

SEE RENAL PAPER NOTES

Drinking Water Example

STARTING SITUATION -ICF: Osmolality is 300 mOsm/kg -ECF: Osmolality is 300 mOsm/kg DRINK WATER: ECF OSMOLALITY FALLS -ICF: Osmolality is 300 mOsm/kg -ECF: Osmolality is 280 mOsm/kg (less concentrated) WATER MOVES DOWN ITS OSMOTIC GRADIENT CELLS SWELLS: ICF FALLS & ECF OSMOLALITY INCREASES -ICF: Osmolality is 293 mOsm/kg -ECF: Osmalility is 293 mOsm/kg

Muscles of anterior fascial compartment of the thigh -Rectus femoris, Vastus medialis, Vastus lateralis and Vastus intermedius all together called as Quadriceps femoris muscle

Sartorius Femoral nerve -Flexes, abducts, laterally rotates thigh at hip joint -Flexes & medially rotates leg at knee joint Iliacus & Psoas -Femoral nerve & lumbar plexus(L1,2,3) -Flexes the thigh at hip joint Pectineus (dual nerve supply) -Femoral nerve and obturator nerve -Flexes and adducts the thigh at hip joint Rectus femoris, Vastus medialis, Vastus lateralis, Vastus intermedius (together form the QUADRICEPS FEMORIS) *These muscles insert as one tendon to the upper part of the patella, then continues down the patella as LIGAMENTUM PATELLAE -Femoral nerve -Extension of leg at knee joint

Hypertonic Saline or Excess Salt Ingestion effect on body water spaces

Scenerio 1: Hypertonic Saline HYPERTONIC SALINE enters ECF -> ECF volume increases, ECF osmolality increases -> water leaves cells down osmotic gradient -> ICF volume decreases, ICF osmolality increases Scenario 2: Ingestion of Excess NACL Ingestion of Excess NaCl -> Increased ECF osmolality -> Water leaves cells down osmotic gradient -> Decreased ICF volume and Increased ICF osmolality

Sciatic Nerve

Sciatic Nerve has 2 components: 1. Tibial Nerve -> Posterior compartment of leg 2. Common Peroneal (fibular) Nerve: a. Deep Peroneal nerve -> Anterior compartment of leg b. Superficial Peroneal Nerve -> Lateral compartment of leg

Water excretion overview

See RENAL PAPER NOTES All water reabsorption passive, 2° to solute reabsorption (i.e. osmosis). When tubule is permeable, tubular fluid isotonic to adjacent interstitium

Water balance

See RENAL PAPER NOTES Obligatory loss: necessary to excrete normal solute content (~500 ml) Facultative loss: excretion of "extra" fluid intake

Shenton's line

Smooth line from the pubis to the neck of the femur seen in the a NORMAL XRAY. If this is altered, concerns for fx By joining the medial margin of the femoral neck and the inferior margin of the superior ramus of pubis, a smoothly curved Shenton's line is visible. Fracture of neck of femur or dislocation of hip joint distorts this line.

Blood urea nitrogen (BUN) This substance is dependent on the GFR and it is very useful in measuring GFR (along with creatinine which we talked about) -What we are really measuring when we measure urea is NITROGEN

Source -deamination of amino acids of dietary protein; -BUN depends on protein intake *Dietary protein will increase UREA level, and if you are protein deficient then it will decrease Effect of GFR -freely filtered & ~50% reabsorbed (facilitated diffusion) -↓ GFR →↑ BUN -BUN depends on GFR (see next slide) Effect of hydration state -BUN reabsorption increases as ADH level increases -i.e. dehydration (↑ osmolality or ↓ volume) →↑ BUN -BUN depends on hydration state -ADH stimulates WATER and UREA reabsorption -Anything that raises ADH will also cause you to have more urea reabsorption so therefore instead of excreting 50% of what was filtered, now maybe you'll only excrete 30% *If BUN increases and NOT creatinine, then its dehydration. ADH stimulates urea reabsorption but doesnt stimulate creatinine

Regulation of H+ secretion

Stimulants of H+ secretion: Increased partial pressure of CO2 Decreased arterial pH Increased plasma aldosterone concentration Increased plasma angiotensin II concentration depletion of body K+ administration of loop or thiazide-like diuretics Inhibitors of H+ secretion Decreased P.CO2,Increased arterial pH, Decreased aldosterone, Decreased angiotensin II administration of K+ sparing diuretics

Thirst & water satiety

Stimuli for thirst: Increased plasma osmolality (sensitive <2% change) Decreased blood volume (relatively insensitive >10% change) Increased angiotensin II (Dr. J Fitzsimons) dry mouth Sensation of satiety: return to normal osmolality & blood volume drinking (before correcting osmolality) oral/GI tract receptors Note: stimuli for thirst are similar to stimuli for ADH release thirst receptors in hypothalamus, but distinct from ADH receptors ADH response more sensitive than thirst

Cutaneous innervation

Superficial Fibular Nerve & Deep Fibular Nerve

Nerves and vessels under cover Gluteus maximus

Superior Gluteal Nerve -> Gluteus Medius and Minimus *Above the PIRIFORMIS Sciatic Nerve *Below the PIRIFORMIS Inferior Gluteal Nerve -> Gluteus Maximus, is just lateral to the sciatic nerve -More medially, there is the PUDENDAL NERVE

Intramuscular Injection in Gluteus Maximus If you wrongly place your injections into the superior medial quadrant you will injury the SUPERIOR GLUTEAL NERVE (affecting the gluteus medius and gluteus minimus If you wrongly place your injections in the inferior medial quadrant you will injury the SCIATIC NERVE If you put your injection in the INFERIOR LATERAL you will injure the INFERIOR GLUTEAL NERVE innervating the gluteus maximus (Pt will complain that they have difficulty climbing upstairs or getting up from sitting position)

Superior lateral quadrant: No major neurovascular structures, preferred site for intramuscular injection Superior medial quadrant: Superior Gluteal neurovascular bundle, injury results in Abductor lurch *Injury here will lead to paralysis of gluteus medius & minimus muscles -> gluteal gait: WADDLING GAIT -> POSITIVE TRENDELENBURG - Positive trendelenburg sign: If the right gluteus medius & minimus muscles are paralyzed, when the patient is asked to stand on right leg the left side(sound side) pelvis sags/droops. Inferior lateral quadrant: Inferior Gluteal neurovascular bundle, injury results in difficulty climbing stairs or raising from a chair *Will lead to paralysis of gluteus maximus muscle leading to DIFFICULTY CLIMBING STAIRS OR RAISING FROM A CHAIR, and WEAKENED EXTENSION AND LATERAL ROTATION OF THE THIGH Inferior medial quadrant: Sciatic nerve, injury results in foot drop

Commonest Injuries to the humerus -If there is a fracture at the shaft of the humerus, Radial Nerve and PROFUNDA BRACHII ARTERY (Triangular space?) -On exam, you would see the pt with WRIST DROP and weakened extension of the elbow *From the axilla the radial nerve gives innervation to the LONG and MEDIAL HEAD of triceps and at the spiral groove the radial nerve gives innervation to the LATERAL and MEDIAL HEAD of the triceps. So injuring the radial nerve at the spiral groove, long head is completely spared and part of medial head is spared, mostly LATERAL head is affected

Supracondylar fracture -At this level, the MEDIAN NERVE and the BRACHIAL ARTERY are running bye -On examination: -Flexors of the forearm are weakened (not totally paralyzed because FLEXOR CARPI ULNARIS and the medial half of FLEXOR DIGITORUM PROFUNDUS are innervated by ulnar nerve) -Pronation of the forearm paralyzed (due to injury to Pronator Teres and Pronator Quadratos) -Weakened flexion at the wrist with ULNAR DEVIATION (Due to flexor carpi radialis paralyzed) -Thenar muscles paralyzed and atrophied so will be flattened out -HAND OF BENIDICTION -Thumb adducted because it cannot abduct (abductor pollicis, flexor pollicis, and opponsins pollicis - are innervated by median nerve) -Loss of sensation to the finger tips, and lateral 3 1/2 fingers on the palmar side -Because of the brachial artery injured, there will be hematoma in the area but there are some anastomoses -Superior ulnar collateral and inferior ulnar collateral anastomose with inferior ulnar recurrent. Radial recurrent artery also anastomoses with branch of the Profunda brachii too?

Intrinsic Muscles of the Hand

THENAR MUSCLES 1. Opponens Pollicis - Recurrent branch of median nerve 2. Abductor Pollicis Brevis - Recurrent branch of median nerve 3. Flexor Pollicis Brevis - Recurrent branch of median nerve 4. Adductor Pollicis - Deep Branch of Ulnar Nerve HYPOTHENAR MUSCLES 1. Abductor Digiti Minimi - Deep Branch of Ulnar Nerve 2. Flexor Digiti Minimi Brevis - Deep branch of ulnar nerve 3. Opponens Digiti Minimi - Deep branch of Ulnar Nerve LUMBRICALS 1. 1ST and 2ND - Median Nerve - Flex metacarpophalangeal joints and extend interphalangeal joints of 2nd-5th fingers 2. 3RD and 4TH - Deep branch of ulnar nerve - Flex metacarpophalangeal joints and extend interphalangeal joints of 2nd-5th fingers

Body Water Spaces For a lean, 70 kg male

TOTAL BODY WATER: 60% body weight, volume ~42L, broken into: 1. EXTRACELLULAR FLUID -1/3 total body water -Volume ~14L 1a. INTERSTITIAL FLUID -4/5 extracellular fluid -Volume ~11L 1b. PLASMA -1/5 extracellular fluid -Volume ~3L 2. INTRACELLULAR FLUID -2/3 total body water -Volume ~28L 3. TRANSCELLULAR FLUID -Water in bladder, GI tract, eyeballs, gallbladder, etc -Volume ~1.5L

Don't mix "Holy Grail" exchanges with H+ buffering

The "Holy Grail" exchanges occur at the luminal surfaces of collecting duct cells. The H+ for Na+ & K+ exchange occurs in most cells of the body and at the basolateral surfaces of kidney epithelial cells.

Compression of Brachial Artery 5 P signs & symptoms-pallor, pain, puffiness, pulselessness & paralysis.

The cause of compression & spasm of the brachial artery are the •supracondylar fracture of the humerus in which the upper bony fragment is displaced anteriorly •Application of tight plaster cast or tourniquet to the arm •This results in inadequate blood supply to the muscles in the anterior compartment of forearm. •Initially this gives rise to 5 P signs & symptoms-pallor, pain, puffiness, pulselessness & paralysis. •Further reduction in blood supply leads to necrosis & fibrosis of the muscles leading to Volkmann's ischemic contracture, in which flexion contracture of the metacarpophalangeal & interphalangeal joint

Definition of clearance

The clearance of a substance is defined as: the (virtual) volume of plasma which contains the weight of the substance excreted per given time (usually per minute). Where: Cx = clearance of X (ml/min) Px = plasma concentration of X (mg/ml) Ux = urinary concentration of "X" (mg/ml) V. = urine flow rate (ml/min) Then: Cx = Ux x V./Px

Pes planus or flat feet

The plantar calcaneonavicular (spring) ligament supports the head of the talus and thereby maintains the medial longitudinal arch. Laxity of this ligament may result in fallen arches or "flat feet (Pes planus)."

Radial Nerve Injury

The radial nerve can be injured at 3 levels 1. Axilla (level 1) -Can be caused by people with walking with crutches regularly -Drunk person can come and lie on chair with arm hanging (Saturday night palsy) -Can cause inability to extend the elbow joint (heads of triceps are involved at the axilla level - paralysis of triceps) -Can cause inability to extend the wrist joint and fingers (flexors would take over the action and the patient would have WRIST DROP) -Sensations at the arm, forearm, and hand is lost 2. Midshaft of Humerus, spiral groove (Level 2) -Everything from above would be present BUT here you can do weak extension of the elbow because the MEDIAL of the TRICEP has dual innervation and still gets its some innervation at the AXILLA (along with its innervation at the spiral groove). Also, The only thing that is injured here is the LONG HEAD of the triceps - FIX THIS! 3. At the elbow (CUBITAL FOSSA LEVEL) where it is dividing terminally as the SUPERFICIAL and DEEP BRANCH -If a tight bandage or a wrap goes on your cubital region and it compresses the SUPERFICIAL branch of the radial nerve, there will be TINGLING/PINS & NEEDLE sensation on the dorsum of the hand, and if compression is bad there will be tingling in the area/loss of sensation in the area. There would be NO WRIST DROP because the deep branch is not injured here. -If the arm is PIERCED and there is injury to the DEEP NERVE there will be no sensation loss but there will be wrist drop

Therapeutic diuretics (summary)

The site of action of diuretics accounts for their effects & side effects 1. Loop diuretics (furosemide, ethacrynic acid, bumetanide) -act in thick ascending limb of loop of Henle -> Decreased Na+/K+/2Cl- transporter -can cause K+ loss ("K+ wasting") -inhibit Ca++ reabsorption →↑Ca++ excretion 2. Thiazide like diuretics (hydrochlorothiazide, chlorthalidone) -act in distal tubule on Na+/Cl- transporter -can cause K+ loss ("K+ wasting") -stimulate Ca++ reabsorption →↓Ca++ excretion 3. K+ sparing diuretics (amiloride, triamterene, spironolactone) -act on collecting duct principal cells -> Decreased Na+ channel activity Effectiveness: loop diuretics > thiazides >> K+ sparing diuretics

Muscular compartments of the thigh

The thigh is divided into 3 muscular compartiments 1. ANTERIOR - Femoral nerve (branch of the lumbosacro plexus) -Small muscles in the upper part of thigh are FLEXORS of the hip -Large muscles of the thigh are EXTENSORS of the KNEE 2. MEDIAL - Obturator Nerve -Adductors of the thigh 3. POSTERIOR - Tibial Component of the SCIATIC NERVE -FLEXORS of the knee

Mechanisms of afferent arteriole contraction

Two ways: 1. Increased arterial pressure -> MYOGENIC RESPONSE (happens in a few seconds) -> Constriction of afferent arteriole smooth muscle -> Minimal increased renal blood flow & increased glomerular filtrate rate 2. Increased arterial pressure -> TUBULOGLOMERULAR FEEDBACK (happens in about 30 seconds) -> Constriction of afferent arteriole smooth muscle -> Minimal increased renal blood flow & increased glomerular filtrate rate Both responses occur in isolated kidney, therefore: a. no nerves involved b. no hormones involved

Clearance Weight in this case is volume x concentration

The volume of plasma which supplies the weight of a substance that is secreted

Loop of Henle properties (thick limb)

Thick ascending limb -impermeable to water (like the thin ascending limb) -luminal (apical) surface Na+K+2Cl- cotransport (2 active) -basolateral surface Na+K+ ATPase (1 active) -together these transporters can create a 200 mOsm/kg (100 mM NaCl) gradient between lumen and adjacent interstitial fluid -countercurrent flow "multiplies" this gradient: "countercurrent multiplier"

Loop of Henle properties (thin limbs)

Thin descending limb -high permeability to water -low permeability to NaCl -equilibrates with adjacent interstitium by osmotic efflux of water -tubular NaCl concentration increases Thin ascending limb -low permeability to water -high permeability to NaCl -equilibrates with adjacent interstitium by efflux of NaCl -Osmolalities of thin descending & ascending limbs, interstitium & vasa recta (see later) equal at any given level of medulla -The thin limbs deliver a hypertonic tubular fluid to the thick ascending limb, thanks to these passive NaCl & water permeability properties.

Tubular osmolalities (+/- ADH) & % filtrate remaining

Thought? what is the TF/P for creatinine at points along nephron?

Muscles of the Posterior Compartment of Forearm

Thumb - Extensor Pollicis Longus Digits - Extensor Digitorum Index Finger - Extensor Indices Pinky Finger - Extensor Digiti Minimi Carpi - Extensor Carpi ulnaris/radialis longus (up to the distal phalynx) Carpi ulnaris/radialis bravis (up to proximal phalynx) Ebow - Anconius - Extension of the elbow joint All of these muscles are EXTENSORS! 1. Brachioradialis - Radial nerve -Flexes forearm and rotate to midprone position 2. Extensor carpi radialis longus -Radial nerve -Extends and abducts wrist 3. Extensor carpi radialis brevis - Deep branch of Radial nerve -Extends and abducts wrist 4. Extensor digitorum - Deep branch of Radial nerve -Extends fingers and hand 5. Extensor digiti minimi - Deep branch of Radial nerve -Extends little finger 6. Extensor carpi ulnaris - Deep branch of Radial nerve -Extends and adducts wrist 7. Anchonius - Radial nerve -Extends elbow joint 8. Supinator - Deep branch of Radial nerve -Supination of forearm 9. Abductor pollicis longus - Deep branch of Radial nerve -Abducts and extends the thumb 10.Extensor pollicis brevis - Deep branch of Radial nerve -Extends the metacarpophalangeal joint of thumb 11. Extensor pollicis longus - Deep branch of Radial nerve -Extends the distal phalanx of thumb 12. Extensor indices - Deep branch of Radial nerve -Extends the metacarpophalangeal joint of index finger

Superficial muscles of the posterior compartment of leg

Tibial nerve

Extensor retinaculum

Tibialis anterior, Extensor Hallucis longus, Anterior tibial artery, Deep peroneal Nerve, Extensor Digitorum longus, Peroneus tertius

Fracture of medial epicondyle

Ulnar nerve injured -This wil paralyze the FLEXOR CARPII ULNARIS, medial portion of the FLEXOR DIGITORUM PROFUNDUS and all the muscles of the hand except for the thenar muscles and the 1st and 2nd lumbricals -The patient will have sensation loss on the medial 1 1/2 fingers on the dorsal and palmar aspect -Here you would see claw hand of the medial 2 fingers (extension at the MPC joint and flexion at the interphalangeal joints - this has been reversed because of paralysis of the 3rd and 4th lumbricals)

Concept of clearance If you had a substance where all of the substance was secreted out of the peritubular capillaries, then you would say, What volume of plasma would that come from? The volume that was filtered (20%) + the 80% that came out of the efferent arterioles and was completed secreted from that. So if you had a substance that was filtered and completely secreted then its clearance would equal the total renal plasma flow (Like PARA AMINO HYPURIC ACID)! -If you have a substances that is filtered and totally secreted will give you a measure of TOTAL RENAL PLASMA FLOW -If you have a substance that is just filtered, it will give you the GLOMERULAR FITLRATION RATE -Anything else will tell you something about the way the kidney handles that substance. If you look at the clearance of creatinine, you notice it is a little more than the clearance of inulin, so you know some must of been secreted. So by doing experiment on the whole body, you can kind of figure out how the kidney handles that substance

Weight excreted = urinary concentration (mg/ml) x urine flow rate (ml/min) = Ux x V (mg/min) -"Clearance" calculates the weight excreted, and then asks, -"What volume of plasma contains the amount excreted, i.e. "cleared"?" the units of clearance are volume/time, usually ml/min -OR What volume of plasma would we have to clear of this substance in order to provide the weight excreted? *It is not the weight excreted, it's the volume of plasma from which that came -Clearance of inulin: *inulin filtered only, ∴ plasma volume cleared = GFR (volume filtered) -Clearance of creatinine: *creatinine filtered + secreted, ∴ plasma volume cleared = GFR + 10%

D! According to the formula for clearance of PAH, [urine concentration of PAH x urine flow or volume per minute (2880 mL/d/1440 min/d=2 ml/min urine)]/ plasma concentration of Cr), renal plasma flow is 400 mL/min (normal = 600-700 mL/min) and angiotensin is a potent vasoconstrictor, mainly of the efferent arteriole in the kidney. Efferent arteriole constriction increases GFR and decreases RPF, and also increases filtration fraction (FF). PAH clearance is a measure of RPF. Us (or substance x) = 2 mg/mL PAH = 0.01 When using PAH, you are measuring RENAL PLASMA FLOW! *If you placed INULIN in the Us instead of PAH, you would be measuring GLOMERULAR FILTRATION RATE *If you placed CREATININE in the Us instead, you would be measuring GFR that is ~90% accurate

Which of the following is the most likely cause of finding a plasma PAH level of 0.01 mg/mL, urine level of 2 mg/mL and 24-h urine volume 2.88 L in a patient? A. Albuminuria B. Low plasma vasopressin C. High plasma vasopressin D. High plasma angiotensin E. Low plasma atrial natriuretic peptide

Plain X-ray wrist joint

Wrist joint formed by SCAPHOID and LUNATE articulating with the lower end of the RADIUS

Dislocated hip

You can tell if there is a dislocation or not by looking at Shenten's Line -Posterior hip dislocation can give issues with SCIATIC NERVE compression. You would see the muscles of the posterior portion of the thigh with all the muscles of the legs are paralyzed. -Entire leg sensation is lost except for medial aspect of the leg and the foot (because of saphenaous) -In a child, the bones are still growing, so compare it to the other side, could be cartilage and not a fracture

Fractional excretion of sodium (FENa+) - importance

You know that ~99.5% of filtered Na+ is reabsorbed. FENa+ is the ~0.5% which isn't reabsorbed. In the healthy kidney, about 0.5% of filtered Na+ is excreted (FENa+ = 0.5%) Even with extreme Na+ loading only about 2% is excreted (FENa+ = 2%) The failing kidney excretes a relatively large fraction of filtered Na+ FENa+ is therefore an important index of kidney function

Pathological conditions: alkalosis

acute & chronic alkalosis stimulates K+ secretion & excretion

Pathological conditions: acute acidosis

acute acidosis inhibits K+ secretion & excretion After several days metabolic acidosis stimulates K+ secretion & excretion (next slide)

Homeostasis of body K+: changes in K+ intake

and vice versa for a reduction in dietary K+

Posterior drawer sign

backward sliding of the tibia on the femur caused by a rupture of the posterior cruciate ligament

Anterior drawer sign

forward sliding of the tibia on the femur due to a rupture of the anterior cruciate ligament

Adductor/Sub sartorial/Hunters canal The femoral artery runs through the subsartorial canal after the femoral triangle. This canal is seen just below the sartorius muscle Subsartorial or adductor canal -Begins at the tip of the femoral triangle and runs obliquely lower down to the medial side of the thigh in the lower part, to an opening in the adducter magnus muscle (called the adductor hiatus) -The contents in this canal are the continuatino of the femoral artery, femoral vein, and the saphenous nerve, and the nerve to vastus medialis (branch of femoral artery) -WHen you want to ligate the femoral artery, you go into the adductor canal to do so. If you do this, the rest of the leg would get its blood supply from the anastomosis around the knee joint from the branches of the femoral artery and the popliteal artery -If there is popliteal artery aneurism, you want to operate, you would ligate the femoral artery in the adductor canal

• 15 cm long • Middle third of the thigh • Deep to Sartorius muscle Extent: • Apex of femoral triangle • Adductor hiatus of tendon of adductor magnus -Contents: Femoral artery, Femoral vein Saphenous nerve and Nerve to Vastus medialis Clinical application: In treatment of Popliteal aneurysm, the surgeons ligate the femoral artery in sub sartorial canal. The principle of this procedure depends on the existence of anastomotic channels around the knee, through which blood reaches the popliteal artery despite ligation of femoral artery. Surgeon John Hunter was the first to describe the exposure and ligation of femoral artery.

Shoulder separation

• A Shoulder Separation is classified as a SUBLUXATION or DISLOCATION of the ACROMIOCLAVICULAR JOINT (AC) • Usually seen hockey players • It is considered severe when CORACLAVICULAR and ACROMIOCLAVICULAR LIGAMENTS are torn • Tear of CORACLAVICULAR LIGAMENT results in shoulder separation

Anterior cruciate ligament injury

• ACL tears occurs when the knee is hyper extended and over rotated • Most common knee injury seen in Skiing and foot ball • Disruption of ACL allows the tibia to slide anteriorly under the femur, a sign known as Anterior drawer sign • ACL injuries may occur in conjunction with tears of the medial collateral ligament and medial meniscus-collectively referred as unhappy triad

Muscular compartments of Forearm

• Anterior compartment: Flexor - Pronator muscles -Anterior department of the forearm is innervated by the MEDIAN NERVE (with some exceptions) -Median nerve is also called the "Laborer's Nerve" as they do heavy lifting • Posterior compartment: Extensor - Supinator Muscles -Posterior compartment does extensor and supination - done by the RADIAL NERVE

Menisci

• C shaped sheets of fibrocartilage on the articular surface of tibia • Peripheral border is thick attached to the capsule • Inner border is thin and concave and forms the free border • Deepens the articular surface of tibial Condyles to receive the femoral condyles -Medial meniscus is less mobile (firmly fused with the tibial collateral ligament) and more prone to tears. The rupture of the medial meniscus is common in football players. On rupture of medial meniscus, the knee gets locked in the flexed position & swollen due to synovitis -Lateral meniscus is more mobile, since few fibers of popliteus are attached to the posterior horn of lateral meniscus, the muscle pulls the meniscus back if the femur is rotated laterally

Ligaments of Hip joint

• Capsular ligament with synovial membrane • Acetabular labrum (Not a ligament, but cartilage, but placed here because it is considered a part of what strengthens the joint) • Transverse acetabular ligament -The lower part of the acetabulum is not very complete. The notch there is supported by the transverse acetabular ligament • Ligament of head of femur • Ilio-femoral, Ischio-femoral and Pubo-femoral ligaments

Ligaments of the Knee joint

• Capsule • Extra capsular ligament -Ligamentum patellae -Lateral collateral -Medial collateral -Oblique popliteal • Intra capsular ligament -Anterior cruciate -Posterior cruciate -Medial & lateral Menisci

Ligaments

• Capsule-encloses the joint and attached to the articular margins • Deltoid or Medial ligament • Lateral ligament

Fracture Clavicle

• Clavicle is commonly fractured at the junction of MEDIAL 2/3rd and LATERAL 1/3rd . • The 2 fragments are displaced in different directions corresponding to the muscle pull • Medial fragment is displaced upwards due to STERNOCLEIDOMASTOID & lateral fragment is drawn downwards by the WEIGHT OF THE UPPER LIMB. -Fractured clavicle may injure SUBCLAVIAN ARTERY, divisions of BRACHIAL PLEXUS (lower trunk) & PLEURA • The fracture is reduced by pulling the shoulder upward & backward and the correct alignment of the fragments is retained by application of a Figure-8 bandage

Dislocation of the Glenohumeral Joint Shoulder Dislocation: 3 types of Anterior Dislocations: Sub-coracoid, Sub-glenoid, Sub clavicular

• Commonly dislocated by direct or indirect injury • Most dislocations of the humeral head occur in the downward (inferior) direction, described clinically as anterior or (more rarely) posterior dislocations. The head ends up lying anterior or posterior to the glenoid cavity. -Anterior dislocation of the Glenohumeral joint : • occurs most often in young adults, particularly athletes. • caused by excessive extension and lateral rotation of the humerus. • The fibrous layer of the joint capsule and glenoid labrum may be injured. • The strong flexor and adductor muscles of the Glenohumeral joint usually subsequently pull the humeral head anterosuperiorly into a sub coracoid position. Anterior: Sub-coracoid, Sub-glenoid, Sub clavicular • Posterior dislocation is uncommon • Recurrent dislocation

Joint capsule

• Dense fibrous capsule that encloses the joint • Capsule is lined internally by synovial membrane • Attached to: - acetabular labrum medially - intertrochanteric line infront of femur - posterior aspect of neck of femur • The capsule inside gets reflected on the femur as RETINACULA which is carrying the blood vessels into the neck and the head of the femur (does not give support)

Alignment ‐ Trauma

• Dislocation Articular surfaces completely incongruent (Completely out of the joint capsule) • Subluxation Articular surfaces partially incongruent (partially out of the joint capsule)

Ligamentum patellae/Patellar ligament

• It is a continuation of Central portion of quadriceps femoris tendon • Attached to patella and tibial tuberosity -Osgood-Schlatter Disease : Sudden hyperextension of the knee may lead to avulsion fracture of tibial tuberosity with injury to Ligamentum patellae

Fracture Scaphoid Radial artery is in the anatomical snuff box -LUNATE is the most common bone that is dislocated - MEDIAN NERVE gets compressed in CARPAL TUNNEL

• Of all the carpal bones, Scaphoid is the most frequently fractured carpal bone and Lunate is the most commonly dislocated bone. • Results from a fall on the palm when the hand is abducted, the fracture occurring across the narrow part (waist) of the scaphoid • Scaphoid can be palpated in the floor of the anatomical snuff box. In fracture of scaphoid pain & tenderness are felt in the snuff-box. • Pain is felt on the lateral side of the wrist, during dorsiflexion and abduction of the hand. • Initial radiographs of the wrist may not reveal a fracture; often this injury is (mis-)diagnosed as a severely sprained wrist. Radiographs taken 10-14 days later reveal a fracture because bone resorption has occurred there. • Avascular necrosis of the proximal fragment of the scaphoid (pathological death of bone resulting from inadequate blood supply) may occur and produce degenerative joint disease of the wrist

Ligament of head of femur -Hip dislocations do not typically occur anteriorly because the strongest ligament, ILIO-FEMORAL LIGAMENT is present there If there is a femoral neck fracture (seen commonly in elderly women with osteoporosis), when you want to fix this fracture, you can approach it ANTERIORLY (cutting the ILIO FEMORAL LIGAMENT) or POSTERIORLY (cutting the ISCHIO-FEMORAL LIGAMENT)

• Often referred to as the ligamentum teres femoris/ligamentum capitis femoris • Triangular fibrous band • Attachment: -apex-attached to the femoral head at fovea -base-to the transverse acetabular ligament • Stretched in adduction • Relaxed in abduction *Functions to keep the head of the femur inside/in place of the acetabulum and also brings the blood vessels to the head of the femur (Specifically the branch of the OBTURATOR ARTERY to supply the head of the femur - but this artery will become a ligament after puberty) TRUE LIGAMENTS (They actually function to support the joint capsule prevent dislocations) 1.Ilio-femoral ligament: strongest ,Y-shaped, located on anterior aspect of the joint, prevents hyperextension of the joint while standing *The STRONGEST ligament of the hip joint 2.Pubo-femoral ligament: Triangular shaped, located on the antero-inferior aspect of the joint, limits extension and abduction 3.Ischio-femoral ligament: Spiral shaped, located on posterior aspect of the joint, limits extension

Injury to Sciatic nerve

• Sciatica is caused by prolapse of the intervertebral disc, which compresses the lower lumbar & upper sacral nerve roots or cause pressure on the sacral plexus. The patient experiences radiating pain down the posterior aspect of the thigh, posterior & lateral side of the leg and lateral part of the foot • Sleeping foot is due to temporary compression of the sciatic nerve against the femur, at the lower border of gluteus maximus, when a person sits on the hard edge of a chair for a long time • The motor effect of injury to sciatic nerve (posterior dislocation) is paralysis of the muscles of posterior compartment of the thigh and of the leg & foot. There is a sensory loss below the knee except for femoral area

Bones ‐ Trauma

• Searching for fractures Assess cortex and medullary space Key findings of FRACTURE • Cortical disruption • Cortical buckling • Lucent or sclerotic lines

Clinical application: Femoral artery

• Since femoral artery is relatively superficial in position, it is easy to approach the artery for various procedure. To inject radiopaque dye in the arteries of abdomen, the catheter is introduced to femoral artery • It is also favored vessel for coronary angiography or for coronary angioplasty • Sudden occlusion or block in the femoral artery usually occurs due to emboli from the heart (myocardial infarction or thrombi in the left atrium in mitral stenosis) or due to traumatic injury or due to diabetes. It presents as five 'P's' (pain, pallor, paresthesia, paralysis & pulselessness) • Profunda femoris artery is in close proximity of the femoral shaft, it is prone to injury in fracture of femoral shaft

Anterior cruciate ligament

• Strong intracapsular ligament • Attachment: below-anterior intercondylar area of tibia above-posterior part of medial surface of lateral femoral condyle • Function: -Prevents posterior displacement of the femur on the tibia - With the knee joint flexed, it prevents the tibia from being pulled anteriorly

Posterior cruciate ligament

• Strong intracapsular ligament • Attachment: below-posterior intercondylar area of tibia above-anterior part of lateral surface of medial femoral condyle • Function: -Prevents anterior displacement of the femur on the tibia -With the knee joint flexed, it prevents the tibia from being pulled posteriorly

Hip joint

• Synovial joint • Ball and socket variety • Ball-Head of femur • Socket -Acetabulum of hipbone -Lunate surface -Acetabular labrum *Hip joint is more stable than the shoulder joint because the acetabulum is deep like a cub, dislocations are not as common -Margin of the acetabulum is lined by the cartilage called the ACETABULUM LABRUM

Rotator Cuff disorders

• The 2 main disorders of the rotator cuff are - IMPINGEMENT - TENDINOPATHY • The muscle most commonly involved is SUPRASPINATOUS • Swelling of supraspinatus muscle, excessive fluid in subacromial bursa or subacromial bony spurs may produce significant impingement when arm is abducted • The blood supply to supraspinatus tendon is POOR, repeated trauma leads to degenerative changes with calcification of tendon producing extreme pain (painful arc syndrome) • FROZEN SHOULDER: tendinitis involving entire rotator cuff.

Venipuncture in the Cubital Fossa

• The cubital fossa is the common site for sampling and transfusion of blood and intravenous injections • Usually, the median cubital vein or basilic vein is selected • The median cubital vein lies directly on the deep fascia, over the bicipital aponeurosis, which separates it from the underlying brachial artery and median nerve and provides some protection to the latter • Historically, during the days of bloodletting, the bicipital aponeurosis was known as the grace Deux (Fr. grace of God) tendon, by the grace of which arterial hemorrhage was usually avoided • The cubital veins are also a site for the introduction of cardiac catheters to secure blood samples from the great vessels and chambers of the heart. These veins may also used for cardio angiography

Knee joint Apart from flexion and extension there is slight lateral and medial rotation. Therefore it is not purely hinge, it is called a "modified hinge joint"

• Type: Complex synovial joint • Articulations and subtype: -Modified hinge type -Between the medial and lateral condyles of femur and tibia -Plane synovial type Between the patella and femur Fibula is not involved in the knee joint

Axillary Nerve Injury

•Shoulder joint dislocation or fractures at the surgical neck of the humerus. -Surgical neck of the humerus, junction between the head and the shaft of the humerus. This is the site where you see the axillary nerve running, along with a branch of the axillary artery -If there is dislocation of the shoulder joint, it can stretch the axillary nerve (you can also see this in fracture of the surgical neck of the humerus) -You cannot do abduction above 15 degrees, weakness in lateral rotation and anesthesia over the shoulder joint if the axillary nerve is injured •Deltoid muscle paralysis and skin anesthesia over the lateral deltoid region. •Shoulder contour may be lost with time as the deltoid atrophies. • Arm abduction is not possible beyond the first 15 degrees and lateral rotation of the shoulder joint is compromised

Radial Pulse

•Using your middle (long) and index (pointer) fingers, gently feel for the radial artery inside your wrist. •Do not use your thumb to take the pulse because it has a pulse of its own. •Count your radial pulse for a full min.(60 seconds). Radial artery can also be palpated in the "anatomical snuff" box against the scaphoid bone .