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HB2 Final > Week 14 - Renal/LE > Flashcards

Week 14 - Renal/LE Flashcards

1
Q

What are the components of internal K balance?

Of external K balance?

A

internal: intracellular vs extracellular pools
external: intake vs excretion

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2
Q

What things can increase K shifting into the cell?

How is this accomplished?

A
  • insulin and B2 agonists

- increases the activity of the Na/K ATPase

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3
Q

What are the ways to affect internal K balance?

A
  1. insulin and B2 agonists bring K into the cell

2. acid/base status, where acidemia kicks K out (and alkalemia sucks K in)

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4
Q

Where does regulation of external K balance mainly occur?

A

in the kidney

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5
Q

Where can you lose K to, externally?

A
  • kidney
  • GI tract
  • skin
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6
Q

Describe the proximal tubule’s overall role in K balance.

A

it participates in a significant amount of K reabsorption, but is not a site for major regulation

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7
Q

Describe the TAL’s overall role in K balance.

A

it participates in a significant amount of K reabsorption, but is not a site for major regulation

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8
Q

Describe the distal neprhon’s overall role in K balance.

A
  • it secretes K variably, depending upon a lot of factors including the size load
  • it is a major site for K regulation
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9
Q

Where does K secretion occur?

How?

A
  • the principal cells of the late distal tubule and collecting duct
  • K channel in the apical membrane
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10
Q

What maintains the high intracellular K concentration in the principal cells?

A

the Na/K ATPase

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11
Q

Of the 3, where is K concentration the highest:

tubular lumen, inside the principal cell, or ECF?

A

inside the principal cell (thanks to the Na/K ATPase)

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12
Q

What is the negative lumen potential in the principal cell generated by?

A

ENaC

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13
Q

What is the net movement of K in the principal cells?

What things allow for that?

A
  • K secretion via K channels

- electrochemical gradient made by ENaC and the Na/K ATPase

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14
Q

What can lower the drive for K secretion?

A
  • intercellular K concentration decreases
  • lumen K concentration increases
  • lumen potential becomes less negative
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15
Q

What is one of the most important regulators of K secretion?

A

aldosterone

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16
Q

What are the methods in which aldosterone affects K secretion?

A
  1. aldosterone increases the activity of the Na/K ATPase, increasing intracellular K
  2. increase the number of ENaC channels, causing increased reabsorption of Na, leading to an increase in the negative lumen potential
  3. increases the number of K channels in the apical membrane of the principal cell
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17
Q

Why does tubular fluid flow rate have a large effect on K secretion?

A
  • if low/no blood flow, the K equilibrates and K secretion stops
  • if fast flow, the secreted K is swept away and the gradient remains strong, promoting K secretion
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18
Q

What things increase K secretion?

A
  • aldosterone
  • increased dietary K
  • increased Na delivery
  • increased flow rate
  • loop diuretics
  • thiazide diuretics
  • alkalosis
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19
Q

What things decrease K secretion?

A
  • decreased dietary K
  • decreased flow rate
  • K-sparing diuretics
  • acidosis
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20
Q

In regards to ADH, what happens when there is excess free water?

A

this means that serum osmolarity is low, inhibiting ADH release, causing the kidney to produce dilute urine and dump free water (and vice versa for low free water)

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21
Q

Where is the primary target for ADH action in the kidney?

A

the principal cell of the collecting duct

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22
Q

Describe the principal cell when there is no ADH, theoretically.

A

collecting duct will be impermeable to water

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23
Q

Describe the principal cell when there is ADH.

A

ADH stimulates V2 receptors to insert acquaporin2 channels into the apical membrane, making the collecting duct permeable to water

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24
Q

Is ADH an all-or-none phenomenon?

A

no, the more ADH is around the higher the water permeability will be (in varying degrees)

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25
Q

How does ADH help to make a concentrated urine?

A
  • causes aquaporin 2 insertion in principal cells (saving free water from being lost in urine)
  • stimulates NKCC2 in TAL (takes more stuff out of the urine into the medulla, makes hyperosmolar inner medulla)
  • increases reabsorption of urea from the collecting duct into inner medulla (makes hyperosmolar inner medulla)
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26
Q

Why is Na primarily regulated?

A

for ECF volume

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27
Q

Why is free water primarily regulated?

A

for osmolarity (or Na concentration)

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28
Q

What is the kidney’s role in acid/base balance?

A
  1. bicarb reabsorption

2. acid excretion/new bicarb production

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29
Q

What processes are involved in acid excretion/new bicarb production?

A
  • titratable acids

- ammonium generation

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30
Q

Where does bicarbonate reabsorption occur?

How?

A
  • in the proximal tubule (indirect process)
    1. Na/H antiporter secretes H into lumen (+ by ang II), which associates with bicarb to make carbonic acid
    2. carbonic anhydrase makes CO2 and water, pulling more H into the reaction by removing the acid
    3. CO2 and water move into the cell
    4. a different carbonic anhydrase pushes them back into carbonic anhydrase, which immediately dissociates into bicarb and H
    5. bicarb pumped out of basolateral membrane where it diffuses into the blood stream
    6. H is recycled back to the lumen via Na/H antiporter to bind with another bicarb
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31
Q

What is the NET in bicarb reabsorption?

A
  • movement of bicarb from the lumen to the bloodstream
  • no NET acid excretion
  • no generation of new bicarb
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32
Q

What structure can reclaim essentially all of the filtered bicarb?

A

the proximal tubule

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33
Q

What stimulates the activity of the Na/H antiporter in the proximal tubule?
In the collecting duct?

A
  • PT: angiotensin II

- CD: aldosterone

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34
Q

What processes result in net acid excretion?

Where does each occur?

A
  • titratable acids, in the proximal tubule

- ammonium generation, in the proximal tubule

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35
Q

Describe the process of titratable acids.

A
  1. carbonic anhydrase makes carbonic acid from water and CO2 in the proximal tubule cells
  2. carbonic acid immediately dissociates into H and bicarb
  3. H ions are pumped into the lumen via the Na/H antiporter
  4. the H in the lumen is buffered by the phosphate that was previously filtered
  5. the bicarb made uses the bicarb/Na symporter to enter the blood, acting as a buffer there
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36
Q

Which process is more important- titratable acids or ammonium generation?
Why?

A

Ammonium generation, because it is an inducible process where more ammonium can be generated if more acid needs excreted. The phosphate is limited in amount to what was filtered

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37
Q

Describe the process of ammonium generation.

A
  1. glutamine is broken down into ammonium and a-ketoglutarate in proximal tubule cells
  2. a-ketoglutarate is converted to bicarb, which is pumped into the blood
  3. ammonium is pumped into the tubular lumen (the Na/H antiporter doubles as a Na/NH4 antiporter)
  4. pH converts ammonium to ammonia in the tubular fluid
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38
Q

Describe the process of ammonium excretion.

A
  1. water and CO2 make carbonic acid using carbonic anhydrase
  2. carbonic acid dissociates into H and bicarb
  3. bicarb is transported into the blood
  4. H pumped out via the H-ATPase
  5. ammonia combines with H to make ammonium, which is excreted
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39
Q

Where does ammonium generation occur?

Ammonium excretion?

A
  • generation: mostly in the proximal tubule

- excretion: in the intercalated cells of the collecting duct

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40
Q

What simulates the H-ATPase activity?

What process is that transporter important for?

A
  • aldosterone

- ammonium excretion

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41
Q

What is the normal fractional excretion of K?

A

10-20%

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42
Q

Why do thiazide and loop diuretics cause K wasting?

A

they inhibit the Na reabsorption upstream of the collecting duct, causing high Na delivery to the collecting duct, which drives further K secretion by the principal cells

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43
Q

What are the pH limits compatible with life?

A

6.8 to 7.8

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44
Q

What is the net effect of ammonium generation/excretion?

A
  • excretion of acid in urine

- generation of new bicarb to replenish what was consumed buffering metabolic acids in the ECF

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45
Q

Why can hyperaldosteronism be associated with metabolic alkalosis?

A

Aldosterone stimulates the activity of the H ATPase in the distal collecting duct. This pushes more new bicarb into the bloodstream.

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46
Q

What is likely your K state if you have acidosis?

A

hyperkalemia (with acidosis, cells buffer about half of H+ by taking it into the cells – push K+ into ECF for electroneutrality)

if low on total K (urinary/GI losses) and in acidosis, will have artificially normal K in ECF but when acidosis is corrected and take up K again – reveals low K

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47
Q

What is likely your K state if you have alkalosis?

A

hypokalemia (alkalosis makes you reduce H secretion, so dump more K to keep the charge balance)

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48
Q

What defines respiratory acidosis?

A

a PaCO2 over 45 mmHg

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49
Q

What defines respiratory alkalosis?

A

a PaCO2 under 35 mmHg

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50
Q

What defines metabolic acidosis?

A

bicarb concentration less than 22 mEq/L

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51
Q

What defines metabolic alkalosis?

A

bicarb concentration greater than 28 mEq/L

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52
Q

What can cause metabolic acidosis?

What is usually present?

A
  • excess production of acids (ketones, lactic acid, chronic renal failure)
  • ingestion of fixed acids (methanol, ethylene glycol, aspirin)
  • loss of bicarb (GI fluid loss from diarrhea, renal tubule acidosis)

-compensatory respiratory alkalosis: reduces arterial PCO2 and increases the pH towards normal

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53
Q

How do you resolve metabolic acidosis without treatment?

A
  • increased renal generation of new bicarb
  • increased H excretion via NH3 production
  • titratable acid excretion
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54
Q 
Metabolic acidosis:
H?
Bicarb?
Arterial PCO2?
Compensation?
A
  • increased H concentration
  • decreased bicarb concentration
  • decreased arterial PCO2
  • hyperventilation (secondary respiratory alkalosis)
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55
Q 
Metabolic alkalosis:
H?
Bicarb?
Arterial PCO2?
Compensation?
A
  • decreased H concentration
  • increased bicarb concentration
  • increased arterial PCO2
  • hypoventilation (secondary respiratory acidosis)
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56
Q 
Respiratory acidosis:
H?
Bicarb?
Arterial PCO2?
Compensation?
A
  • increased H concentration
  • increased bicarb
  • increased arterial PCO2
  • increased H excretion and increased bicarb generation (renal)
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57
Q 
Respiratory alkalosis:
H?
Bicarb?
Arterial PCO2?
Compensation?
A
  • decreased H concentration
  • decreased bicarb
  • decreased arterial PCO2
  • decreased H excretion and decreased bicarb generation (renal)
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58
Q

How do you calculate the anion gap?

A

Na - (Cl + bicarb)

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59
Q

What is the normal anion gap?

What does that reflect?

A
  • between 8-16 mEq/L

- the concentration of unmeasured anions like protein, phosphate, sulfate, and citrate

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60
Q

When metabolic acidosis is caused by a loss of bicarb, what happens to the anion gap?

A

there is an increase of Cl (hyperchloremic metabolic acidosis) rather than the addition of other unmeasured anions, and the anion gap is normal (b/c ECF is electroneutral at all times in regards to measured anions)

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61
Q

What are the most common causes of metabolic acidosis with an increased anion gap?

A 
(MULEPAK)
Methanol ingestion
Uremia
Lactic acidosis
Ethylene glycol ingestion
Paraldehyde ingestion
Aspirin overdose
Ketoacidosis
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62
Q

What are the most common causes of metabolic acidosis without an increased anion gap?

A 
(Could Really DeHydrate)
Carbonic anhydrase inhibitors
Renal tubular acidosis
Diarrhea
Hyperalimentation (IV feeding)
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63
Q

What are the most common causes of metabolic alkalosis?

A
  • loss of gastric H from vomiting (excess bicarb in blood)
  • contraction alkalosis, a net gain of bicarb by the renal system (bicarb retention occurs as a side effect of low effective circulating volume)
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64
Q

How can low effective circulating volume cause bicarb retention?

A
  • low GFR, reducing the bicarb filtered load

- avid proximal tubular reabsorption regardless of filtered load

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65
Q

What usually accompanies metabolic alkalosis?

A

compensatory respiratory acidosis, where arterial PCO2 increases to try to decrease the pH back to normal

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66
Q

How can you correct metabolic alkalosis without treatment?

A
  • increased renal excretion of bicarb
  • reduced rates of acid excretion
  • reduced rates of bicarb retention
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67
Q

What physiologically causes respiratory acidosis?

A

inadequate alveolar ventilation that results in CO2 retention

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68
Q

What can things can cause respiratory acidosis?

A
  • neuromuscular disorders
  • airway obstruction
  • narcotics that suppress breathing
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69
Q

What happens in chronic respiratory acidosis?

A

the renal system normalizes the pH by excreting more acid and producing more bicarb, which is added to the ECF

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70
Q

What are sensible losses?

A

water loss that we can measure

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71
Q

What are insensible losses?

A

water loss that you cannot measure

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72
Q

What physiologically causes respiratory alkalosis?

A

excessive alveolar ventilation, resulting in greater CO2 loss than production

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73
Q

What can cause respiratory alkalosis?

A
  • high altitude (hypoxemia)
  • pulmonary embolism (hypoxemia)
  • psychogenic hyperventilation
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74
Q

What happens in chronic respiratory alkalosis?

A

the renal system normalizes the pH by excreting less acid and producing less “new” bicarb

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75
Q

What does ‘compensation’ refer to?

A

responses that normalize plasma pH

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76
Q

If both alkalosis and acidosis are present and the pH is acidic, what do you consider the primary disorder?

A

the acidosis (although both are present)

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77
Q

Explain the effects of excessive aspirin ingestion.

A
  • aspirin uncouples os/phos, causing a primary metabolic lactic acidosis
  • directly affects the respiratory centers in the meduall, causing the central chemoreceptors to be more sensitive to arterial PCO2 levels, which cause primary respiratory alkalosis
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78
Q

What does furosamide do?
Where does it act?
How does it work?
K status?

A
  • inhibits the NKCC2
  • the loop of Henle (TAL)
  • decreases the electrochemical gradient, reducing Na, Ca, and Mg reabsorption
  • K wasting, because lower electrochemical gradient by the time it gets to the collecting duct
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79
Q

What are the K wasting diuretics?

A

loop and thiazide

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80
Q

What are the anterior ligaments of the hip joint?

Posterior ligaments?

A
  • anterior: iliofemoral (Y shape) and pubofemoral

- posterior: ischiofemoral

81
Q

What is the strongest ligament in the body?

Where is it located?

A
  • the iliofemoral ligament

- the anterior hip joint

82
Q

What gives the blood supply to the femoral head and neck?
Where does it come off of?
Where are they located?

A
  • the lateral and medial circumflex femoral arteries
  • off of the profunda femoris artery
  • in the intertrochanteric groove
83
Q

What is the most common type of hip fractures?

What is healing like, and why?

A
  • intertrochanteric hip fractures

- they heal better than other types because of denser bone and better blood supply

84
Q

What is healing like for a femoral head fracture?

Why?

A
  • very difficult to heal
  • because a fracture at the neck comprimises the blood supply from the circumflex femoral arteries, which can lead to avascular necrosis
85
Q

Why are 75% of hip replacements performed?

A

hip osteoarthritis

86
Q

How do hip dislocations commonly present?

What is a common mechanism that would cause this?

A
  • with the leg adducted and internally rotated

- falls, car crashes (knee hitting dash board), etc

87
Q

What is contained in the superficial fascia of the lower limb?

A
  • cutaneous nerves
  • superficial epigastric artery
  • external pudendal artery
  • great saphenous vein
  • superficial inguinal lymph nodes
88
Q

What is the IT tract made of?

A

it is a thickened continuation of the fascia lata

89
Q

What is the blood supply to the posterior thigh?

A

only via 4 small perforating arteries (from the deep artery of the thigh) that pass through the adductor magnus

90
Q

What is the deep artery of the thigh aka?

A

the profunda femoris artery

91
Q

What is the chief blood supply to the anterior thigh?

A

the profunda femoris artery (off of the femoral)

92
Q

What does the femoral artery become after leaving the anterior thigh?

A

the popliteal artery

93
Q

What vein parallels the femoral artery in the thigh?

A

the deep vein of the thigh (aka profunda femoris vein)

94
Q

What does the great saphenous vein drain into?

A

the femoral vein

95
Q

What does the deep vein of the thigh drain into?

A

the femoral vein

96
Q

Where do most lymph nodes in the leg drain into?

A

the superficial inguinal lymph nodes

97
Q

Where do all of the hamstring muscles come off of?

A

a common head on the ischial tuberosity

98
Q

What are the muscles of the posterior compartment of the thigh?
What are they aka?

A
  • biceps femoris
  • semitendinosus
  • semimembranosus

-aka hamstrings

99
Q

What innervates the hamstrings?

What is the exception?

A
  • the tibial division of the sciatic nerve

- short head of biceps femoris: common fibular division of the sciatic nerve

100
Q

What are the muscles in the anterior compartment of the thigh?

A
  • iliopsoas
  • quadriceps femoris
  • sartorius
101
Q

What are the components of the quadriceps femoris?

A
  • rectus femoris
  • vastus medialis
  • vastus intermedius
  • vastus lateralis
102
Q

What are the muscles of the medial compartment of the thigh?

A
  • obturator externus
  • pectineus
  • gracilis
  • adductor longus
  • adductor brevis
  • adductor magnus
103
Q

Where does the iliopsoas insert?

A

the lesser trochanter of the femur

104
Q

What is the job of the muscles in the medial compartment of the thigh?
Where do these muscles live?

A
  • adduction of the thigh (mostly)

- in the groin

105
Q

What are the boundaries of the femoral triangle?

A
  • roof: fascia lata
  • floor: iliopsoas and pectineus
  • top: inguinal ligament
  • lateral side: sartorius
  • medial side: adductor longus
106
Q

What lives inside the femoral triangle?

A

(NAVEL, from lateral to medial)

  • femoral Nerve
  • femoral Artery
  • femoral Vein
  • Empty space
  • deep inguinal Lymph nodes
107
Q

Why is the empty space in the femoral triangle important?

A

it is where femoral hernias can occur

108
Q

What is the adductor canal aka?

What are the openings at either end?

A
  • subsartorial canal, or Hunter’s canal

- the apex of the femoral traingle and the adductor hiatus

109
Q

What runs in the adductor canal?

What continues on through the adductor hiatus and what does not?

A
  • femoral artery and vein (continue through the adductor hiatus)
  • saphenous nerve (continues on, but not through the adductor hiatus)
110
Q

What are the boundaries of the popliteal fossa?

What lives in there?

A
  • semimembranosus, gastrocnemius medial and lateral heads, and the biceps femoris
  • Contents: tibial nerve, common fibular nerve, popliteal artery and vein
111
Q

Describe the knee joint capsule.

A
  • outer layer: external fibrous layer

- inner layer: internal synovial membrane

112
Q

What are the collateral ligaments of the knee?

What bone do they attach to?

A
  • medial collateral ligament (MCL): tibia

- lateral collateral ligament (LCL): fibula

113
Q

Which collateral ligament is more robust and attaches to the meniscus?

114
Q

What are the cruciate ligaments of the knee?

A
  • anterior cruciate ligament (ACL)

- posterior cruciate ligament (PCL)

115
Q

Which direction does the ACL run?

A

from lateral to medial

116
Q

Where are the ACL and PCL located in relation to the internal synovial membrane?
Why is this important?

A
  • ACL is almost completely enveloped and surrounded by synovium, and the PCL is mostly surrounded
  • blood supply is very poor here, causing difficulty healing tears of these ligaments
117
Q

Describe the medial meniscus.

Describe the lateral meniscus.

A
  • medial: C shaped, attached to tibia, MCL attaches to it

- lateral: O shaped (mostly)

118
Q

What motion frequently causes ACL tears?

What else can easily be damaged?

A
  • external rotation of the femur on the tibia, running and cutting sharply, landing on a straight knee
  • the medial meniscus (they are attached)
119
Q

Describe a 1st degree ligament injury.

A

some pain, minimal swelling, no loss of function

120
Q

Describe a 2nd degree ligament injury.

A

moderate tear, pain, moderate loss of function, swelling, slight instability

121
Q

Describe a 3rd degree ligament injury.

A

complete tear, pain, loss of function, severe instability

122
Q

What is the function of the PCL?

How can you injure it?

A
  • prevents posterior movement of the tibia on the femur

- falling on a flexed knee, or knee meets dashboard

123
Q

What happens when you apply Valgus stress to the leg?

A

push the foot laterally from the knee

124
Q

What happens when you apply Varus stress to the leg?

A

push the foot medially from the knee

125
Q

If you apply Valgus stress to the knee, what will tear?

Common mechanism of injury?

A
  • MCL

- athlete’s knee hit from the outside

126
Q

If you apply Varus stress to the knee, what will tear?

Common mechanism of injury?

A
  • LCL

- opponent lands on inside of athlete’s knee

127
Q

Where does the saphenous cutaneous nerve innervate?

A

roughly the medial calf area

128
Q

Where does the cutaneous portion of the deep fibular nerve innervate?

A

the webbing between the 1st and 2nd toes

129
Q

What vein drains the medial part of the leg?

Where does it drain into?

A
  • the great saphenous vein

- into the femoral vein

130
Q

What vein drains the posterior part of the leg?

Where does it drain into?

A
  • the small saphenous vein

- the popliteal vein

131
Q

Where is the great saphenous vein located in relation to the malleolus?

A

the vein runs medial to the malleolus

132
Q

Where is the crural fascia of the leg very tight over?

Why is this a concern?

A
  • the anterior and lateral compartments

- could cause compartment syndrome

133
Q

What muscles are in the anterior compartment of the leg?

A
  • tibialis anterior
  • extensor digitorum longus
  • extensor hallucis longus
  • fibularis tertius
134
Q

What muscles are in the lateral compartment of the leg?

A
  • fibularis longus

- fibularis brevis

135
Q

What muscles are in the superficial posterior compartment of the leg?

A
  • soleus
  • gastrocnemius
  • plantaris
136
Q

What muscles are in the deep posterior compartment of the leg?

A
  • tibialis posterior
  • flexor digitorum longus
  • flexor hallucis longus
  • popliteus
137
Q

What does the flexor retinaculum create?

What runs through there?

A
  • the tarsal tunnel

- tibial nerve, posterior tibial artery, medial plantar artery, and medial plantar nerve

138
Q

What artery feeds the anterior compartment of the leg?

What nerve is located in the anterior compartment?

A
  • the anterior tibial artery

- the deep fibular nerve

139
Q

Outline the artery branching from external iliac down.

A

external iliac
femoral artery
popliteal
anterior tibial (to dorsalis pedis) and posterior tibial (to medial/lateral plantar arteries and fibular artery)

140
Q

Once you cross the ankle, what does the anterior tibial artery become?

A

the dorsalis pedis artery

141
Q

What does the deep fibular nerve innervate?

A
  • the anterior compartment of the leg

- the webbing between the 1st and 2nd toes

142
Q

What is the anterior compartment of the leg aka?

A

the dorsiflexor (extensor) compartment

143
Q

What nerve innervates the lateral compartment of the leg?

What artery is in the lateral compartment?

A
  • the superficial fibular nerve

- there is no artery in this compartment

144
Q

Injury to what can cause foot drop?

How can this injury occur?

A
  • the common fibular nerve or the deep fibular nerve

- fracture to the proximal fibula

145
Q

What is the posterior compartment of the leg aka?

A

the plantarflexor compartment

146
Q

What nerve innervates the posterior compartments of the leg?

What artery supplies that area?

A
  • the tibial nerve

- fibular and posterior tibial arteries

147
Q

What motions does the talocrural joint allow for?

What motions does the subtalar joint allow for?

A
  • talocrural: plantarflexion and dorsiflexion

- subtalar: inversion and eversion

148
Q

What is the most commonly injured ligament in the body?

A

the anterior talofibular ligament

149
Q

What are the important lateral ligaments of the ankle?

A
  • anterior talofibular ligament
  • posterior talofibular ligament
  • calcaneofibular ligament
150
Q

Biceps femoris:
Action?
Innervation?
Compartment?

A

-action: flexion and lateral rotation of the knee; extension of the hip (long head)

  • long head: tibial division of the sciatic nerve
  • short head: common fibular division of the sciatic nerve

-compartment: posterior of thigh

151
Q

Semitendinosus:
Action?
Innervation?
Compartment?

A
  • action: flexion and medial rotation of the knee; extension of the hip
  • innervation: tibial division of the sciatic nerve
  • compartment: posterior of thigh

(same as semimembransosus)

152
Q

Semimembranosus:
Action?
Innervation?
Compartment?

A
  • action: flexion and medial rotation of the knee; extension of the hip
  • innervation: tibial division of the sciatic nerve
  • compartment: posterior of thigh

(same as semitendinosus)

153
Q

Sartorius:
Action?
Innervation?
Compartment?

A
  • action: flexion, lateral rotation, and abduction of the hip, flexion of the knee (hackey sack)
  • innervation: femoral nerve
  • compartment: anterior of thigh
154
Q

Quadriceps muscles:
Action?
Innervation?
Compartment?

A
  • action: lateralis, medialis, and intermedius do extension of the knee; femoris does extension of the knee and flexion of the hip
  • innervation: femoris, lateralis, and intermedius by the femoral nerve; medialis by the nerve to the vastus medialis (a branch of the femoral nerve)
  • compartment: anterior of thigh
155
Q

Iliopsoas:
Action?
Innervation?
Compartment?

A
  • action: flexion of the hip
  • innervation: femoral nerve
  • compartment: anterior of thigh
156
Q

What innervates the anterior compartment of the thigh?

A

the femoral nerve

157
Q

Pectineus:
Action?
Innervation?
Compartment?

A
  • action: adduction and flexion of the hip
  • innervation: femoral nerve
  • compartment: medial of thigh
158
Q

Adductor longus and brevis:
Action?
Innervation?
Compartment?

A
  • action: adduction and flexion of the hip
  • innervation: obturator nerve
  • compartment: medial of thigh
159
Q

Adductor magnus:
Action?
Innervation?
Compartment?

A

Superior fibers:

  • action: adduction and flexion of the hip
  • innervation: posterior branch of the obturator nerve

Inferior fibers:

  • action: adduction and extension of the hip
  • innervation: tibial division of the sciatic nerve

-compartment: medial of thigh

160
Q

Gracilis:
Action?
Innervation?
Compartment?

A
  • action: adduction of the hip; flexion and medial rotation of the knee
  • innervation: obturator nerve
  • compartment: medial of thigh
161
Q

Obturator externus:
Action?
Innervation?
Compartment?

A
  • action: lateral rotation of the hip
  • innervation: obturator nerve
  • compartment: medial of thigh
162
Q

Tibialis anterior:
Action?
Innervation?
Compartment?

A
  • action: dorsiflexion of the ankle; inversion of the foot
  • innervation: deep fibular nerve
  • compartment: anterior of leg
163
Q

Extensor hallucis longus:
Action?
Innervation?
Compartment?

A
  • action: extension of the MTP and IP joints of the hallux; dorsiflexion of the ankle
  • innervation: deep fibular nerve
  • compartment: anterior of leg
164
Q

Extensor digitorum longus:
Action?
Innervation?
Compartment?

A
  • action: extension of MTP and IP joints of toes 2-5; dorsiflexion of the ankle
  • innervation: deep fibular nerve
  • compartment: anterior of leg
165
Q

Fibularis (peroneus) tertius:
Action?
Innervation?
Compartment?

A
  • action: eversion of the foot; dorsiflexion of the ankle
  • innervation: deep fibular nerve
  • compartment: anterior of leg
166
Q

Fibularis longus and brevis:
Action?
Innervatin?
Compartment?

A
  • action: eversion of the foot; plantarflexion of the ankle
  • innervation: superficial fibular nerve
  • compartment: lateral of leg
167
Q

Gastrocnemius and Plantaris:
Action?
Innervation?
Compartment?

A
  • action: plantarflexion of the ankle; flexion of the knee
  • innervation: tibial nerve
  • compartment: superficial posterior of leg
168
Q

Soleus:
Action?
Innervation?
Compartment?

A
  • action: plantarflexion of the ankle
  • innervation: tibial nerve
  • compartment: superficial posterior of leg
169
Q

Popliteus:
Action?
Innervation?
Compartment?

A
  • action: unlocks the fully extended knee at the beginning of flexion by laterally rotating the femur; flexion and medial rotation of the knee
  • innervation: tibial nerve
  • compartment: deep posterior of leg
170
Q

Flexor hallucis longus:
Action?
Innervation?
Compartment?

A
  • action: flexion of MTP and IP joints of the hallux; inversion of the foot; plantarflexion of the ankle
  • innervation: tibial nerve
  • compartment: deep posterior of leg
171
Q

Tibialis posterior:
Action?
Innervation?
Compartment?

A
  • action: inversion of the foot; plantarflexion of the ankle
  • innervation: tibial nerve
  • compartment: deep posterior of leg
172
Q

Flexor digitorum longus:
Action?
Innervation?
Compartment?

A
  • action: flexion of the MTP, PIP, and DIP joints of toes 2-5; inversion of the foot; plantarflexion of the ankle
  • innervation: tibial nerve
  • compartment: deep posterior of leg
173
Q

What nerve innervates the anterior compartment of the thigh?

A

the femoral nerve

174
Q

What does the obturator nerve innervate?

A
  • adductor longus
  • adductor brevis
  • half of the adductor magnus
  • gracilis
  • obturator externus
175
Q

What nerve innervates the anterior compartment of the leg?

A

the deep fibular nerve

176
Q

What nerve innervates the lateral compartment of the leg?

A

the superficial fibular nerve

177
Q

What nerve innervates the posterior compartment of the leg?

A

the tibial nerve

178
Q

What action is common to both tibialis anterior and tibialis posterior?

A

inversion of the foot

179
Q

Where does most of the total body calcium reside?

A

in the calcium salts that make up bone

180
Q

How much of the total body calcium is easily measurable?

Where is it located?

A
  • about 0.1%

- in the ECF

181
Q

What symptoms are associated with hypocalcemia?

A

seizures, muscle spasms, excitability, generalized muscle weakness

182
Q

What symptoms are associate with hypercalcemia?

A

depression, lethargy, coma, constipation, muscle weakness, kidney stones, increased urine output (bones, stones, moans, groans, and psychiatric overtones)

183
Q

In what forms and percentages is Ca located in the ECF?

Which is the one that is regulated?

A
  • 40% protein bound (mostly to albumin)
  • 50% ionized/free (regulated)
  • 10% complexed
184
Q

When you say hypocalcemia, what are you specifically looking at?

A

low free/ionized Ca in the blood

185
Q

Under what conditions would it be helpful to be in a positive Ca balance?

A
  • children
  • pregnant women
  • people with broken bones
186
Q

What is the form of vitamin D that you can personally generate?

A

D3, cholecalciferol

187
Q

Explain the process of vitamin D activation.

A

the kidney converts 25-D3 to 1,25-D3 using 1a-hydroxylase in a highly regulated process

188
Q

What are the effects of calcitriol in regards to Ca?

Which one is the most significant effect?

A
  • increases Ca absorption in the GI tract (most)
  • increases Ca reabsorption in the kidney (moderate)
  • increases bone mineralization (minor)
189
Q

What activates 1a-hydroxylase?

190
Q

What is active vitamin D a strong suppressor of?

A

PTH production

191
Q

How does PTH secretion work?

A
  • if there is high Ca, CaSR senses this and blocks the release of PTH
  • if there is low Ca, the stimulus is removed, the suppression is removed, and PTH is released
192
Q

What are the effects of PTH in regards to Ca balance?

What is the largest effect?

A
  • tells osteoblasts to talk to osteoclasts to start bone resorption (largest)
  • increases Ca reabsorption in the kidney
  • activates vitamin D by stimulating 1a-hydroxylase
  • increases GI absorption of Ca
193
Q

Where in the nephron is the bulk of Ca reabsorbed?

A

the proximal tubule

194
Q

How can you regulate Ca reabsorption in the TAL?

A

furosemide blocks Ca reabsorption

195
Q

How can you regulate Ca reabsorption in the distal nephron?

A
  • PTH increases reabsorption of Ca

- thiazide diuretics increase reabsorption of Ca

196
Q

What things stimulate PTH release?

A
  • low Ca

- high phosphate

197
Q

What does PTH do in regards to phosphate balance?

What is the net?

A
  • increases production of activated vitamin D via 1a-hydroxylase. However, increased serum phosphate downregulates 1a-hydroxylase, so this is a wash.
  • increases bone resorption
  • decreases kidney reabsorption of phosphate (leave more in the urine)
  • production of FGF23 from bone is stimulated, which also decreases phosphate reabsorption in the kidney and blocks 1a-hydroxylase

-net is loss of K, because the kidney dumps more than is released from the bone

198
Q

Where is most of the phosphate balance regulated in the nephron?
Why?

A
  • in the proximal tubule

- there is not significant transport of phosphate in any other part of the neprhon

HB2 Final (5 decks)

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