Physiology

Front 1

Case_27
How does kidney respond to metabolic acidosis vs metabolic alcalosis?

Back 1

Excretes more fixed hydrogen in form of ammonia and reabsorbs more bicarbonate vs reverse for alcalosis.

Front 2

Case_27
How would you correct an DKA in the ER?

Back 2

Two large-bore IV lines with 2L of isotonic solution with insulin drip. DKA can have an underlying etiology (eg infection)

Front 3

Case_27
Give examples of normal anion gap acidosis vs increased anion gap acidosis (do ABG's to find out the anion gap)

Back 3

Metabolic acidosis can be devided into two groups: normal and abnormal anion gap acidosis. Examples of nL: renal tubular acidosis and GI bicarb loss (diarrhea). ABnL: injestion of EtOH, methanol or ethylene glycol, salicylates, cyanide, paraldehyde, uremia/renal failure, lactic acidosis, DKA and alcoholic ketoacidosis.

Front 4

Case_27
How do you calculate anion gap?

Back 4

Na - (Cl + bicarb) if bicarb goes down, Cl goes up to compensate -nL mechanism. If foreign cation is present then bicarb goes down while Cl 'doesn't know about it in the presence of a foreign cation'-> increased anion gap

Front 5

Case_27
What is the nL pH of plasma?

Back 5

7.4

Front 6

Case_27
what is the difference b/w carbonic (fatty acids and carbs) and non-carbonic (phospholipids and sulfur containing amino acids) acid?

Back 6

carbonic acid's products of metabolism are CO2 and water, vs non-carbonic->non-volatile acid

Front 7

Case_27
What are the four lines of defenses against an acid or base challenge?

Back 7

1)Albumin and Hgb, bicarb - simple buffers, react upon contact.
2)Intracellular-H+ is pulled inside the cell and K+ is going out (slower than 1))
3)Pulmonary compensation- MINIMIZES changes in pH (does not restore) neural central and peripheral chemoreceptors that control resp rate - immediate response
4)Kidney response- RESTORES pH balance (while pulm minimizes); chemoreceptors sensitive to H+, CO2 and O2-> regulates secretion, reabsorption, etc. Tightly coupled with pulmonary response b/c sensitive to arterial CO2. Slowest to react to changes.

Front 8

Case_27
explain log bicarb/co2, i.e. log kidney/lung

Back 8

Ration is most important: if ration goes UP (i.e. bicarb up or co2 down)->alcalosis and vica versa

Front 9

Case_27
noncarbonic or fixed acids (proteins and phospholipids) vs carbonic acids (fats and carbs). What happens to the end products?

Back 9

carbonic-Co2 and water (breath out, pee out). fixed-nonvolatile sulfuric acid and phosphoric acid to be peed out, i.e. kidney regulation entirely (would explain the need for a protein free diet in kidney failure)

Front 10

Case_47
What is the location of lesion in a patient with Hemibalismus, Hungtington's and Parkinson's?

Back 10

Subthalamic nucleus, striatum and substantia niagra (SSS)

Front 11

Case_47
Where are basal ganglia located. Name five basal ganglia. What is one of their functions?

Back 11

Below Thalamus. Caudate nucleus, putament, GP-globus palidus, subthalamic nucleus and substantia niagra. They provide a motor loop

Front 12

Case_47
What is the major INHIBITORY neurotransmitter for the brain and for spinal cord/brain stem?

Back 12

Gamma-aminobutiric acid (GABA) -brain. Glycine- for brain stem and spinal cord.

Front 13

Case_47
Role of D1 dopamine receptors and D2 receptors?

Back 13

D1->Direct pathway (no synapse)-facilitates movement-produces EXCITATION.
D2->InDirect pathway (one synapse)- inhibits movement-produces INHIBITION.

Front 14

Case_47
What pathways are important in schizophrenia? Where do they arise from?

Back 14

Mesolimbic and mesocortical tracts that arise from substantia niagra.

Front 15

Case_47
How does Huntington's disease start and progress?

Back 15

It is a heritable hyperkinetic disease: loss of inhibitory neurons (that give rise to inhibitory pathway) in striatum

Front 16

Case_51
What does rebound pain means?

Back 16

Peritoneal irritation

Front 17

Case_51
What is the sympathetic response to low volume?

Back 17

Increased TPR, increased HR and increased contractility.

Front 18

Case_51
describe the response of Renin-Angiotensine-Aldosterone-System RAAS. What does ADH do? What does Renin do?

Back 18

Increase in Angiotensine II leads to increase TPR and increase in Aldosterone, which in turns increases of Sodium-Chloride reabsorption in kidney to increase volume. Vasopressin - increase vasoconstriction and increase in aquaporin channels to facilitate water reabsorption in the kidney. Renin- conversion of tensinogen to Aldosterone I (then ACE converts Aldosterone I to Aldosterone II).

Front 19

Case_51
How do we know that the kidneys are being adequately perfused?

Back 19

Check the output (production of urine)

Front 20

Case_51
What is the Mean Arterial Pressure have to be to consider circulatory shock (failing to perfuse periphery)

Back 20

MAP<70mmHg DP+ 1/3(SP-DP)

Front 21

Case_51
Where are the low pressure baroreceptors and high pressure baroreceptors located?

Back 21

High pressure - aortic arch, carotid artery and AFFerent arteriole (renal). LOW pressure - in ATRia and PULMOnary Veins

Front 22

Case_51
What portion of kidney is in charge of NaCl reabsorption stimulated by Aldosterone?

Back 22

Cortical Collecting DUCT of the kidney

Front 23

Case_51
Where dose ADH come from? Function?

Back 23

Posterior pituitary. Vasopressin-increase vasoconstriction and increase in aquaporin channels to facilitate water reabsorption in the kidney.

Front 24

Case_51
When does irreversible shock happen? What's the mechanism?

Back 24

Ischemic tissue releases metabolitea that serve as vasodilators that counteract the effects of vasoconstrictors, thus, even though you may restore the volume, the pressure won't climb back to due to irreversible damage to the tissue. At some point the heart muscle starts releaseng toxic metabolites that won't allow the heart's recovery-death is imminent, i.e. Cardiac Output is not re-established. I.e. CO is the most critical.

Front 25

Case_51
What is a better way to re-establish the blood volume in less severe cases? More severe cases?

Back 25

Colloid free (no plasma for oncotic pressure) metabolic fluids- Ringer's Lactate. More severe?-> plasma and whole blood with volume expanders.

Front 26

Case_51
What is the mcc of peripheral edema in post-shock cases?

Back 26

Capillaries become leaky with plasma proteins going through (not supposed to normally). Such diffuse capillary leakage is the primary reason for peripheral edema regardless of which resuscitation fluid is used.

Front 27

Case_51
What is the best immediate therapy for a person in hemorrhagic shock?

Back 27

Administer isotonic crystalloid colloid-free solution - NS (normal saline) until RBCs are available (blood bank has to match bld type first). restore hemodynamics first, b/c Hct loss of up to 20% can be tolerated . I.e. avoid the pnt going into irreversible shock.

Front 28

Case_51
What is the primary defect in circulatory shock?

Back 28

Inadequate Cardiac OUTPUT (CO), not just MAP<70mmHg

Front 29

Case_51
How does body fends off drop in MAP? Name 5 mechanisms.

Back 29

Sympathetic response! Baroreceptor reflex! Carotid bodies! RAAS! ADH release.

Front 30

Case_18
What is the utility of PFT Pulmonary Function Test?

Back 30

Measures lung capacity and airflow rates

Front 31

Case_18
Give examples of the conditions that will decrease one's Functional Residual Capacity? How would you qualify such a detriment?

Back 31

It is a restrictive lung problem. Dzs: neuromuscular problem, pleural dz, chest wall problem, decreased lung compliance.

Front 32

Case_18
What is hypoxemia and how is it caused? How is hypoxia different?

Back 32

Decreased partial pressure of O2 in the blood, i.e. O2 deficiency. Caused due to thickening of alveolar membrane-> diffusion distance increased. Hypoxia is deficiency of O2 reaching the tissues, despite adequate perfusion of the tissues, i.e. mismatch in O2 supply and demand.

Front 33

Case_18
Restrictive vs Obstructive. PFT can distinguish, but clinical presentation is most important.

Back 33

THICKNESS greater (thus distance for diffusion is increased)-increase in work necessary for lung expansion vs AREA for perfusion is inadequate (asthma, emphysema, bronchitis) due to airway resistance-narrowing passages due to inflammation or compression.

Front 34

Case_18
Sarcoidosis

Back 34

Chronic injury- noncaseating granuloma in bronchioles and alveolar sacs, chronic, resulting in fibrotic tissue

Front 35

Case_18
What is the interplearual pressure?

Back 35

The elastic recoil of the lung to collapse on itself and the outward recoil of the chest wall create the PRESSURE. During expansion of the chest wall interpleaural pressure decreases causing expansion of the lung.

Front 36

Case_18
Define compliance vs elasticity

Back 36

Change of volume over pressure. It is (inverse of elasticity -ability to return to the original shape after the stress is removed, i.e. elastic recoil). eg Fibrotic lung with small compliance but high elasticity

Front 37

Elasticity and FRC (functional residual capacity). Forced Expiratory Volume, FRV1 (over 1 second)

Back 37

FRC is lower with high elasticity (nL ~2300ml), i.e. fibrotic lung- restrictive dz (vs obstructive). Neuromuscular dz (prevents expansion of muscles), scoliotic dz (chest deformity), pneumothorax- no full expansion of the lung. FEV and FEV1 are low, thus ration FEV1/FEV may be normal.

Front 38

Case_18
What is the utility of N2O in a pneumothorax?

Back 38

N2O is the fastest diffusing gas across pulmonary membrane. Thus, in pneumothorax give some N2O to fill the pleural leak and N2O will be reabsorbed->the lung will expand completely.

Front 39

Case_18
Perfusion vs diffusion

Back 39

If a gas like N2O or O2 have enough time to diffuse through the membrane to bind to Hgb with the membrane that has a normal thickness, then all we need is blood to increase the content of gas- PERFUSION limitation. In DIFFUSION limitation the area of surface and thickness of the barrier become and issue, which creates an ALVEOLAR-ARTERIAL O2 gradient (since we talk about O2)

Front 40

Case_18
If FRC is increased, and FEV1 is decreased, what could be the cause?

Back 40

One of the causes may be dynamic compression of the airway (obstructive dz)

Front 41

Case_18
PFTs indicate FEV1 78% and FVC 70%. What type of the dz is it?

Back 41

Restrictive (high elasticity and low compliance, i.e. change of volume over change in pressure).

Front 42

Case_18
What gas is the most diffusion limited and which is the most perfusion limited. What gasses are intermediate?

Back 42

CO. N2O. CO2 and O2

Front 43

Case_18
How do you correct diffusion limitation of O2?

Back 43

Increase O2 concentration in inspired air, i.e. give pt 100% oxygen

Front 44

Case_26
What element is secreted less with ACE-I administered? And how significant that is?

Back 44

Potassium-> hyperKalemia (increase in extracellular environment). It decreases excitability of the heart - the most significant effect.

Front 45

Case_26
What leads to HyperKalemina?

Back 45

Crush injury, burn, excessive exercise (increased K load); Acidosis and insulin deficiency (shifts in/out cell); Adrenal insufficiency (Addison dz); Pseudohyperkalemia (hemolysis of blood sample); Hypoaldosteronism; decreased renal secretion (renal failure, ACE-I, K-sparing diuretics-spironolactone and eplerenone)

Front 46

Case_26
Treatment of hyperkalemia i.e. >5.5 (while continuously monitoring EKG/ECG)

Back 46

Insulin (drives K intracellular), bicarb (alkalinizes bld forcing K to move from outside inside the cell)

Front 47

Case_26
What is the normal K?

Back 47

3.5-5.5 mEq/L

Front 48

Case_26
MOA of mineralcorticoid Aldosterone

Back 48

increases Na reabsorption and K secretion in cortical collecting duct and initial collecting tubule

Front 49

Case_26
What is the hormone that plays a critical role in controlling metabolism of Magnesium, Calcium and Phosphate

Back 49

PTH

Front 50

Case_26
What is the main regulation between ECF and ICF compartments mechanism of K+? Total body?

Back 50

Na/K pump (ATPase); the other- Na-K exchange (less understood); total body - by urinary excretion.

Front 51

Case_26
Effects of pH on K+

Back 51

Alkalosis drives H+ out of the cell and K+ inside - thus decreasing K+ ECF (extracellular levels) eg hyperventilation, high altitude, whatever makes you alkalotic

Front 52

Case_26
What is the role of K+?

Back 52

regulation of muscle resting potential, cardiac function; regulation of protein and glycogen synthesis; INTRAcellular pH

Front 53

Case_26
What are the major players that drive K+ inside the cell

Back 53

insulin and Aldosterone

Front 54

Case_26
Total body regulation of K+

Back 54

K+ is regulated with kidney secretion and further excretion in urine- i.e. if dietary intake is high. Great 80% are reabsorbed in proximal tubule and Loop of Henle. Hypovolemia/dehydration make RAAS kick in-> Aldosterone UP and K+ is secreted. HyperK can stimulate Aldosterone

Front 55

Case_26
Role of Calcium

Back 55

muscle contraction, hormone secretion, proliferation and gene expression

Front 56

Case_26
Ca balance achieved how?

Back 56

Absorbed in intestines; excreted in kidneys; released and uptaken by bone. Regulated by PTH, D3, calcitonin and plasma Ca levels

Front 57

Case_26
major regulator of Ca reabsorption and where is Ca reabsorbed in kidney?

Back 57

PTH; thick ascending limb and distal convoluted tubule.

Front 58

Case_26
How do PTH and calcitonin act through on Ca reabsorption? What is the intermediate?

Back 58

AdeNYLYL cyclase and cyclic adenosine monophosphate (cAMP)

Front 59

Case_26
What are the dominant sites of K+ regulation (i.e. secretion) vs reabsorption?

Back 59

initial collecting tubule and cortical collecting duct to secrete K+, but reabsorption takes place in proximal tube and the Loop of H.