Physiology

Question 1

Which segment of the systemic circulation has the greatest resistance to flow?

Answer 1

Arterioles. Arterioles contribute the largest part of the TPR (aka SVR).

Question 2

compression atelectasis

Answer 2

Occurs with accumulation of blood, fluid, or air within the pleural cavity, which mechanically collapses the lung.

Question 3

contraction atelectasis + clinical significance

Answer 3

1) Occurs when fibrosis of lung or pleura prevent full expansion.
2) atelectasis type post radiation.

Question 4

resorption atelectasis

Answer 4

Caused by obstruction. Remaining air in alveoli gets resorbed.

Question 5

alveolar dead space

Answer 5

Sum of volumes of those alveoli which are ventilated but not perfused.

Question 6

anatomic dead space

Answer 6

Normal dead space. Portion of airway which conducts gas to the alveoli.

Question 7

physiologic dead space

Answer 7

Sum of anatomical dead space plus alveolar dead space.

Question 8

Dead space

Answer 8

Air that is inhaled in gas exchange but does not participate in gas exchange either because it 1) remains in the conducting airways or 2) reaches alveoli that are not perfused or poorly perfused.

Question 9

Pulmonary shunt

Answer 9

Condition in which alveoli of lungs are perfused as normal but ventilation fails to supply perfused region.

Question 10

Lab values in mixed metabolic acidosis and respiratory alkalosis (eg late stage salicylate poisoning)

Answer 10

Acidotic with low bicarb, low pCO2.

Question 11

ACTH stimulation test (adrenocorticotropic stimulation test)

Answer 11

Test used to determine renal functioning.

Question 12

Diabetic diarrhea pathophys

Answer 12

Autonomic neuropathy, leading to motility disorder.

Question 13

metabolic acidosis cause

Answer 13

1) Increased production of hydrogen ions or
2) inability of body to form bicarbonate.
Thus, in either case, bicarbonate is LOW.

Question 14

Lab values in DKA

Answer 14

hyperglycemia + increased hydrogen ions + depleted HCO3- + increased ketones + leukocytosis

Question 15

Shilling test

Answer 15

used to confirm that parietal cells aren’t producing sufficient IF to support B12 absorption. In first stage, give radiolabeled oral B12 + an injection of unlabeled B12. The single injection temporarily saturates B12 receptors in the liver with enough normal B12 to prevent radioactive B12 binding in body tissues, so that if absorbed from the GI tract, it will pass into the urine. Thus, low excretion suggests poor absorption of B12 (it is passed into feces rather than absorbed and excreted in urine). In second stage, give radiolabeled oral B12 + IF. If this is normal, then person has a lack of intrinsic factor, or pernicious anemia. A low result implies malabsorption.

Question 16

contraction alkalosis pathophys

Answer 16

a few things contribute

1) renal compensation for volume loss. RAAS–> ang II –> increased Na-H exchange in proximal tubule and increased HCO3- reabsorption
2) Aldosterone induces H+ efflux
3) loss of solvent volume without a proportional loss in bicarb concentration.

Question 17

Pendrin

Answer 17

Chloride/bicarbonate exchange in the collecting duct.

Question 18

Pauci-immune

Answer 18

Vasculitis associated with minimal evidence of hypersensitivity upon immunofluorescence., eg churg straus, wegeners, microscopic polyangiitis.

Question 19

Formation of brownstones

Answer 19

Bacteria have glucoronidases that can deconjugate biluribin. Conjugated bilirubin isn’t a problem because it can dissolve and come out.

Question 20

Why is BUN/Cr high in prerenal AKI?

Answer 20

Urea is necessary to create a gradient in the collecting tubule for water reabsorption. Thus, with hypovolemia, you have increased ADH production, causing increased urea reabsorption. Creatinine is never absorbed, so relatively the ratio is increased.

Question 21

Fever mechanism

Answer 21

Pyrogens –> increased IL-1 –> IL-1 acts on anterior hypothalamus to increase prostaglandins –> prostaglandins increase the set-point temperature. This also explains why aspirin reduces fever (by inhibiting COX-1, prostaglandins can’t increase the set-point).

Question 22

inside of cell vs. outside of cell

Answer 22

inside is negative, which is why sodium depolarizes cell.

Question 23

SGLT-1 expressed where?

Answer 23

gut. That’s why you need to give glucose in rehydration solutions.

Question 24

Difference between SLGT-1 and GLUT-2?

Answer 24

Glucose taken up by SGLT-1. Transported to blood by GLUT-2.

Question 25

what solutions cause cell lysis?

Answer 25

hypotonic

Question 26

acetylcholine action at muscle end plate…

Answer 26

Opens BOTH Na and K+ ion channels. Thus, membrane potential is depolarized to a value that is approximately halfway between respective membrane potentials.

Question 27

How do inhibitory postsynaptic potentials hyper polarize the postsynaptic membrane?

Answer 27

Opening Cl- channels (remember Cl- is concentrated OUTSIDE the cell).

Question 28

secondary active transport

Answer 28

(cotransport) Indirect ATP. Uses a Na+ gradient as an energy source, and therefore, uses ATP indirectly. eg SGLT-1

Question 29

What causes rigor?

Answer 29

ATP is depleted –> no ATP bound, thus myosin remains attached to actin and cross-bridge cycle cannot continue.

Question 30

Why does hyperkalemia cause muscle weakness?

Answer 30

Elevated K+ depolarizes the equilibrium potential and therefore depolarization of the resting membrane potential in skeletal muscle. Sustained depolarization closes the inactivation gates on Na+ channels and prevents the occurrence of action potentials in the muscle.

Question 31

Why do you get amenorrhea with hyperthyroidism?

Answer 31

Increased SHBG –> leading to decreased estrogen.

Question 32

Why do you hypocholesteromia in hyperthyroidism?

Answer 32

Thyroid hormone upregulates LDL receptors.

Question 33

how does acetazolamide cause diuresis? acidosis? hyperventilation?

Answer 33

carbonic anhydrase sits on the apical side of the tubule and converts carbonic acid to H2O and CO2 –> CO2 diffuses into cell combines with H20 in cell to reform carbonic acid –> carbonic acid converted again to release H+ ions, which are exchanged with sodium. Without being able to generate Hydrogen ions inside the cell, sodium can’t be reabsorbed and is diuresed. Without being able to reform bicarb inside the cell and transport it to blood, the patient becomes acidotic, this is what explains metabolic acidosis. Similarly, patient hyperventilates, which is why it can be used for altitude sickness.

Question 34

Why is there a spike in FSH accompanying LH?

Answer 34

Estradiol synthesis has a positive feedback effect on synthesis of FSH and LH.

Question 35

Magnesium in relation to PTH

Answer 35

Hypo or hypermagnesemia can impair PTH secretion or responsiveness, leading to hypocalcemia. But slightly reduced Mg can increase PTH but really reduced Mg inhibits it.

Question 36

When does shunt physiology occur?

Answer 36

1) pulmonary edema
2) pneumonia
Lungs are normally perfused but not ventilated because of fluid buildup

Question 37

NBME explanation for PCOS

Answer 37

Excess adipose causes higher levels of estrogen because estrone is aromatized to estrogen, which inhibits the LH surge.

Question 38

Positive progestin challenge means…

Answer 38

Anovulation