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Step 1 Complete > Physio 2 USMLE > Flashcards

Physio 2 USMLE Flashcards

1
Q

Tidal volume

A

Volume of air that enters and leaves the lung in a single cycle. 500ml

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2
Q

Functional residual capacity

A

Amount of air in the lungs after passive expiration. 2,700ml

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3
Q

Inspiratory capacity

A

Maximal volume of gas inspired from FRC. 4,000ml

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4
Q

Inspiratory reserve volume

A

Air that can be inhaled after normal inspiration. 3,500ml

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5
Q

Expiratory reserve volume

A

Air that can be expired after a normal expiration. 1,500ml

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6
Q

Residual volume

A

Air in the lungs after maximal expiration. 1,200ml

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7
Q

Vital capacity

A

Maximal air that can expired after maximal inspiration. 5,500ml

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8
Q

Total lung capacity

A

Air in the lungs after maximal inspiration. 6,700ml

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9
Q

Total ventilation

A

Total ventilation = Tidal volume X respiratory rate.

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10
Q

Dead space

A

Regions that contain air but do not exchange O2 and CO2

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11
Q

Anatomic dead space

A

Conducting zones. Approximately equal to person’t weight in pounds.

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12
Q

Alveolar dead space

A

Alveoli with air but without blood flow

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13
Q

Physiologic dead space

A

Anatomic dead space plus alveolar dead space

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14
Q

Alveolar ventilation

A

Tidal volume - anatomic dead space X respiratory rate.

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15
Q

Lung recoil

A

Force that collapses the lung. As the lung enlarges, recoil increases and vice versa.

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16
Q

Intrapleural pressure

A

Normally -5 cmH2O. Force that expands the lung. The more negative, the more lung expansion.

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17
Q

Lung mechanics before inspiration

A

Glotis is open but no air is flowing - alveolar pressure = 0. Intrapleural pressure and lung recoil are equal but opposite. Gravity increases intrapleural pressure at the apex and decreases it at the bases. Apex alveoli are more distended.

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18
Q

Lung mechanics during inspiration

A

Diaphragm contracts, intrapleural pressure becomes more negative. Expansion of alveoli makes alveolar pressure negative causing air to flow into the lungs.

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19
Q

Lung mechanics at the end of inspiration

A

Intrapleural pressure and recoil are the same but opposite. Alveolar pressure returns to zero and air stops flowing in.

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20
Q

Lung mechanics during expiration

A

Diaphragm relaxes, intrapleural pressure increases, lung recoil collpases the lung. Alveoli compress the air and alveolar pressure becomes positive and air flows out of the lungs until alveolar pressure is back to zero. Lung recoil and intrapleural pressure become equal but opposite.

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21
Q

Assisted control mode ventilation

A

Inspiration is initiated by the patient or the machine if no signal is detected.

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22
Q

Positive end-expiratory pressure

A

Does not allow intraalveolar pressure to return to zero at the end of expiration. The larger lung volume prevents atelectasis.

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23
Q

What is lung compliance?

A

It’s the change in volume with a change in pressure. Increased compliance means more air flows in with a given change in pressure. Decreased compliance means the opposite. The steeper the slope of the lung inflation curve, the greater the compliance. Emphysema = very compliant; fibrosis = not compliant.

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24
Q

Components of lung recoil

A

1) the tissue’s collagen and elastin fibers and 2) the surface tension (greatest component)

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25
Q

Functions of surfactant

A

Lowers lung recoil and increases compliance (↓ surface tension) more in small alveoli than large alveoli; reduces capillary filtration forces reducing tendency to develop edema.

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26
Q

Pathophysiology of respiratory distress syndrome

A

Low surfactant –> ↑ recoil, ↓ compliance (a greater change in intrapleural pressure is necessary to inflate the lungs); alveoli collapse (atelectasis); more negative intrapleural pressures promote capillary filtration (pulmonary edema)

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27
Q

Airway resistance

A

R = 1/r4; first and second bronchi have less radius than alveoli, therefore more resistance. Ach increases resistance (bronchoconstriction), catecholamines decrease resistance (bronchodilation)

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28
Q

Effect of lung volume on airway resistance

A

↑ lung volume –> ↑ radius –> ↓ resistance. The more negative the intrapleural pressure, the less resistance

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29
Q

Lung volumes in obstructive disease

A

↑ TLC, ↑ RV, ↑ FRC, ↓ FEV1, ↓ FVC, ↓ FEV1/FVC

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30
Q

Lung volumes in restrictive disease

A

↓ TLC, ↓ RV, ↓ FRC, ↓ FEV1, ↓ FEV, ↑ FEV1/FVC

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31
Q

Pressure of alveolar O2 and CO2

A

PAO2 = 100mmHg; PACO2 = 40mmHg

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32
Q

Pressure of venous pulmonary capillary O2 and CO2

A

PvO2 = 40mmHg; PvCO2 = 47mmHg

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33
Q

Pressure of arterial pulmonary capillary O2 and CO2

A

PO2 = 100mmHg; PCO2 = 40mmHg

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34
Q

Which factors affect PCO2?

A

Metabolic CO2 production and alveolar ventilation

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35
Q

Relationship between alveolar ventilation and PACO2

A

Inversely proportional. Hyperventilation decreases PACO2; hypoventilation increases PACO2.

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36
Q

Relationship between PAO2 and PACO2

A

↓ PACO2 –> ↑ PAO2 (hyperventilation); ↑ PACO2 –> ↓ PAO2 (hypoventilation)

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37
Q

Which factors affect PAO2?

A

Atmospheric pressure, oxygen concentration of inspired air and PACO2

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38
Q

What determines oxygen content?

A

Hemoglobin concentration. 1.34ml O2 combines with each gram of hemoglobin.

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39
Q

Amount of dissolved oxygen in the blood

A

0.3 volumes %; 0.3ml per 100ml of blood. Determines PO2 which acts to keep oxygen bound to Hb

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40
Q

What determines oxygen attachment to hemoglobin?

A

PO2 and the affinity of the individual attachment sites. The higher the affinity, the less PO2 is needed to keep it attached

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41
Q

What determines PO2?

A

Amount of oxygen dissolved in plasma. Normally 0.3 volumes %.

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42
Q

Site 4 of hemoglobin

A

Oxygen is attached at 100mmHg. Least affinity, last site to be saturated.

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43
Q

Site 3 of hemoglobin

A

Oxygen is attached at 40mmHg. More affinity than site 4, less affinity than site 2.

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44
Q

Site 2 of hemoglobin

A

Oxygen is attached at 26mmHg which is p50. More affinity, second site to be saturated.

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45
Q

Site 1 of hemoglobin

A

Oxygen remains attached under physiologic conditions. Highest affinity, first site to be saturated.

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46
Q

Factors that shift oxygen dissociation curve to the right

A

↑ CO2, ↑ 2,3BPG, fever, acidosis

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47
Q

Factors that shift oxygen dissociation curve to the left

A

↓ CO2, ↓ 2,3BPG, hypothermia, alkalosis, HbF, methemoglobin, carbon monoxide, stored blood

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48
Q

How is CO2 carried in the blood?

A

5% dissolved; 5% attached to Hb (carbamino compounds); 90% as bicarbonate.

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49
Q

Main drive for ventilation

A

H+ ions from dissociated H2CO3 which stimulate central chemoreceptors. H2CO3 is proportional to PCO2 of CSF

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50
Q

Central chemoreceptors

A

Sense [H+] which is proportional to PCO2 and H2CO3 of the CSF (not systemic)

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51
Q

Peripheral chemoreceptors

A

Carotid bodies (afferents via IX), aortic bodies (afferents via X). Monitor PO2 and [H+/CO2]

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52
Q

Main drive for ventilation in severe hypoxemia

A

Peripheral chemoreceptors sense PaO2 (dissolved oxygen) once PaO2 falls to 50-60mmHg.

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53
Q

Ventilatory response to chronic hypoventilation

A

Peripheral chemoreceptors are the main drive for ventilation eventhough PaCO2 is increased.

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54
Q

Ventilatory response to anemia

A

PaO2 and PACO2 are normal, therefore neither peripheral nor central chemoreceptors respond.

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55
Q

Central control of ventilation

A

Apneustic center in the caudal pons promotes prolonged inspiration. Pneumotaxic center in the rostral pons inhibits apneustic center. Efferents are from the medulla to the phrenic nerve (C1-C3) to the diaphragm

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56
Q

Differences in ventilation between the base and the apex of the lung

A

Base intrapleural pressure is -2.5, alveoli are compliant and small with a small volume of air but receive a large amount of ventilation; Apex pressure is -10, alveoli are large and stiff and contain a large volume of air but receive small amount of ventilation.

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57
Q

Differences in blood flow between the base and the apex of the lung

A

Blood vessels of the apex are less distended, have more resistance and receive less blood flow. Blood vessels of the base are more distended, have less resistance and receive more blood flow

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58
Q

Ventilation/perfussion relationship at the base of the lungs

A

Blood flow is higher than ventilation, the relationship is less than 0.8; the bases are underventilated, ↑ shunts

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59
Q

Ventilation/perfusion relationship at the apex of the lungs

A

Blood flow is lower than ventilation, the relationship is more than 0.8; the apex are overventilated, ↑ dead space

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60
Q

What does a ventilation/perfussion relationship under and over 0.8 mean?

A

Under 0.8 (at the bases) lungs are underventilated and less gas exchange takes place, therefore PACO2 and end-capillary PCO2 will be higher and PAO2 and end-capillary PO2 will be lower.

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61
Q

What is hypoxic vasoconstriction?

A

A decrease in PAO2 causes vasoconstriction and shunting of blood through that segment.

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62
Q

What is the effect of a thrombus in a pulmonary artery?

A

Blood flow decreases, therefore ↑ Va/Q –> ↓ PACO2, ↑ PAO2

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63
Q

What is the effect of a foreign object occluding a terminal bronchi?

A

Ventilation decreases, therefore ↓ Va/Q –> ↑ PACO2, ↓ PAO2

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64
Q

What constitutes a pulmonary shunt?

A

Regions of the lung where blood is not ventilated. Low Va/Q relationship.

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65
Q

What constitutes alveolar dead space?

A

Regions of the lung where there’s no blood flow in spite of ventilation. High Va/Q relantionship

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66
Q

Va/Q > 0.8

A

Represents alveolar dead space. Can be reversed with supplemental O2

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67
Q

Va/Q < 0.8

A

Represents a pulmonary shunt. Cannot be reversed with supplemental O2

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68
Q

What is the normal A-a gradient?

A

5-10 mmHg

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69
Q

Hypoventilation

A

↓ PAO2 but diffusion and A-a gradient are normal. Perfusion-limited defect.

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70
Q

What is a perfusion-limited defect?

A

There’s a lung problem but A-a gradient is normal

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71
Q

What is a diffusion-limited defect?

A

There’s a lung problem where A-a gradient is below normal, therefore diffusion isn’t normal

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72
Q

Diffusion impairment lung defect

A

Due to structural problem (↑ thickness or ↓ surface area). A-a gradient is more than normal. Supplemental oxygen compensates structural deficit but increased A-a gradient remains. Fibrosis, emphysema.

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73
Q

Diffusion capacity of the lung

A

Its measured with CO because it’s a diffusion-limited gas. Structural problems decrease CO uptake. It’s an index of surface area and membrane thickness.

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74
Q

Pulmonary right-left shunt

A

↓ Va/Q. There is an increased A-a gradient that is unresponsive to supplemental O2. Atelectasis or ARDS.

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75
Q

PO2 in atrial septal defect

A

↑ Right atrial PO2, ↑ right ventricular PO2, ↑ pulmonary artery PO2, ↑ pulmonary blood flow and pressure

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76
Q

PO2 in ventricular septal defect

A

No change in right atrial PO2, ↑ right ventricular PO2, ↑ pulmonary artery PO2, ↑ pulmonary flow and pressure

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77
Q

PO2 in patent ductus arteriosus

A

No change in right atrial PO2 nor right ventricular PO2, ↑ pulmonary artery PO2, ↑ pulmonary flow and pressure

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78
Q

Effect of sympathetic stimulation in the GI tract

A

↓ motility, ↓ secretions, ↑ contraction of sphincters

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79
Q

Effect of parasympathetic stimulation in GI tract

A

↑ motility, ↑ secretions, ↑ relaxation of sphincters (except LES which contracts), ↑ gastrin release

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80
Q

Hormones of the GI system

A

Gastrin, CCK, secretin, GIP

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81
Q

Stimulus for gastrin secretion

A

Stomach distension. Stomach acid in the duodenum inhibits gastrin release

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82
Q

Sources of gastrin

A

G cells of the stomach, antrum, duodenum

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83
Q

Actions of gastrin

A

Stimulates acid secretion by parietal cells, increases motility and secretions.

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84
Q

Source of secretin

A

S cells of the duodenum

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85
Q

Stimulus for secretin release

A

Acid entering the duodenum

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86
Q

Actions of secretin

A

Stimulates HCO3 secretion by pancreas to neutralize acid entering duodenum

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87
Q

Source of CCK

A

Cells lining the duodenum

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88
Q

Stimulus for CCK secretion

A

Fat and amino acids entering duodenum

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89
Q

Actions of CCK

A

Inhibits gastric emptying, stimulates pancreatic enzyme secretion, stimulates contraction of the gallbladder and relaxation of sphincter of Oddi.

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90
Q

Source of GIP

A

Duodenum

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91
Q

Stimulus for GIP secretion

A

Fat, carbs and amino acids

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92
Q

Actions of GIP

A

Inhibits stomach motility and secretion

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93
Q

Properties of GI smooth muscle

A

Stretch stimulates contraction, electrical syncytium with gap junctions, pacemaker activity

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94
Q

Factors that inhibit gastric motility

A

Acid in the duodenum (secretin), fat in the duodenum (CCK), hypoerosmolarity in duodenum, distension of duodenum

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95
Q

Factors that stimulate gastric motility

A

Distension of the stomach and ACh

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96
Q

What are the different contractions of the intestines?

A

Segmentation contractions (mixing), peristaltic movements (propulsive).

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97
Q

What factors control the ileocecal sphincter?

A

Distension of the ileum relaxes, distension of the colon contracts

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98
Q

What are the different contractions of the colon

A

Segmentation contractions (haustrations), peristalsis and mass movements

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99
Q

Composition of salivary secretions

A

Low in NaCl because of reabsorption; High in K and HCO3 because of secretion; alpha-amylase begins digestion of carbs; fluid is hypotonic due to NaCl reabsorption and impermeability of ducts to water

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100
Q

Parietal cells

A

Located in the middle part of the gastric glands. Secrete HCl and intrinsic factor.

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101
Q

Chief cells

A

Located in the deep part of the gastric glands. Secrete pepsinogen which is converted to pepsin by acid medium. Pepsin begins digestion of proteins to peptides

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102
Q

Mucous cells of the stomach

A

Located in the superficial part if the gastric glands (gastric pits). Secrete mucus and HCO3. Secreteion is stimulated by PGE2

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103
Q

Ionic composition of gastric secretions

A

High in H+, K+ and Cl-, low in Na+. Vomiting produces metabolic alkalosis and hypokalemia.

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104
Q

Control of acid secretion

A

Acetylcholine, histamine and gastrin stimulate parietal cells to secrete acid.

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105
Q

Secretion of acid by parietal cells

A

CO2 is extracted from the blood and combined into H2CO3 by carbonic anhydrase. H+ ions are exchanged by the proton pump for K+ ions (active antitransport)

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106
Q

Pancreatic amylase

A

Hydrolyzes α-1,4-glucoside bonds forming α-limit dextrins, maltotriose and maltose

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107
Q

Pancreatic lipase

A

Needs colipase which displaces bile from surface of micelles. Lipase digests triglycerides to two free fatty acids and one 2-monoglyceride

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108
Q

Cholesterol esterase

A

Hydrolizes cholesterol esters to yield cholesterol and free fatty acids

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109
Q

Pancreatic proteases

A

Trypsinogen is converted to trypsin by enterokinase –> chymotrypsinogen is converted to chymotrypsin by trypsin –> procarboxypeptidase is converted to carboxypeptidase by trypsin

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110
Q

Ionic composition of pancreatic secretions

A

Isotonic due to permeability of ducts to water and high in HCO3. Stimulated by CCK and secretin.

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111
Q

What are the primary bile acids?

A

Cholic acid and chenodeoxycolic acid. Synthesized in the liver from cholesterol.

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112
Q

How are bile salts formed?

A

Bile acids (cholic and deoxycholic) are conjugated with glycine and taurine which mix with cations to form salts.

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113
Q

What are the secondary bile acids?

A

Formed by deconjugation of bile salts by enteric bacteria - deoxycholic acid (from cholic acid) and lithocolic acid (from chenodeoxycholic acid). Lithocholic acid is hepatotoxic and is excreted.

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114
Q

Enterohepatic circulation

A

Bile acids are reabsorbed only in the distal ileum. Resection or malabsoption syndromes lead to steatorrhea and cholesterol gallstones.

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115
Q

What are the components of bile?

A

Conjugated bile acids (cholic and chenodeoxycholic), billirubin, lecithin and cholesterol.

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116
Q

How are carbohydrates absorbed?

A

Glucose and galactose via active secondary Na cotransporter. Fructose is absorbed independently

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117
Q

How are amino acids absorbed?

A

Secondary active transport linked to Na and receptor-mediated endocytosis.

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118
Q

How are lipids absorbed?

A

Micelles diffuse to the brush border then digested lipids (2-monoglycerides, fatty acids, cholesterol and ADEK vitamins) diffuse into enterocytes. Triglycerides are resynthesized and packaged as chylomicrons with apoB48. Leave the intestine via lymphatics to thoracic duct.

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119
Q

↑ glomerular pressure, ↓ peritulbuar pressure, ↓ RPF

A

Efferent arteriole constriction

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120
Q

↓ glomerular pressure, ↑ peritubular pressure, ↑ RPF

A

Efferent arteriole dilation

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121
Q

↓ glomerular pressure, ↓ peritulbuar pressure, ↓ RPF

A

Afferent arteriole constriction

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122
Q

↑ glomerular pressure, ↑ peritulbuar pressure, ↑ RPF

A

Afferent arteriole dilation

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123
Q

Afferent arteriole dilation

A

↑ glomerular pressure, ↑ peritulbuar pressure, ↑ RPF, ↑ GFR

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124
Q

Afferent arteriole constriction

A

↓ glomerular pressure, ↓ peritulbuar pressure, ↓ RPF, ↓ GFR

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125
Q

Efferent arteriole dilation

A

↓ glomerular pressure, ↑ peritubular pressure, ↑ RPF, ↓ GFR

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126
Q

Efferent arteriole constriction

A

↑ glomerular pressure, ↓ peritulbuar pressure, ↓ RPF, ↑ GFR, ↑ FF

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127
Q

Plasma oncotic pressure changes as blood flows through the nephron

A

Oncotic pressure increases because filtered fluid increases protein concentration. Oncotic pressure is resposible for peritubular reabsorption

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128
Q

Normal capillary hydrostatic pressure of the glomerulus

A

45 mmHg

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129
Q

Normal capillary oncotic pressure of the glomerulus

A

27 mmHg

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130
Q

Normal hydrostatic pressure of bowman’s capsule

A

10 mmHg

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131
Q

Normal GFR value

A

120 ml/min

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132
Q

Normal RPF value

A

600 ml/min

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133
Q

Normal filtration fraction value

A

FF = GFR/RPF = 120mi/min / 600ml/min = 0.20

134
Q

Effect of sympathetic stimulation in the nephron

A

↓ GFR, ↑ FF, ↑ peritubular reabsoption

135
Q

Effect of angiotensin II in the kidney

A

Vasoconstriction of the efferent arteriole more than afferent –> maintains GFR

136
Q

Filtered load

A

Rate at which a substance filters into Bowman’s capsule = FL = GFR x Free plasma concentration

137
Q

Excretion of a substance in the urine

A

Excretion = filtered load + (amount secreted - amount reabsorbed) = filtered load + transport OR urine concentration X urine flow rate

138
Q

Characteristics of a Tm system

A

Carriers become saturated, carriers have high affinity, low back leak. The filtered load is reabsorbed until carriers are saturated - the excess is excreted.

139
Q

Renal treshold for glucose

A

180 mg/dl or 1.8 mg/ml. Represents the beginning of splay.

140
Q

Tm rate of reabsorption of glucose

A

375 mg/min. Represents the maximum filtered load that can be reabsorbed when all carriers in the kidney are saturated (end of splay region).

141
Q

Glucose reabsorption graph

A

At normal glucose levels, the amount filtered is the same as the amount reabsorbed. At treshold (beginning of splay), the excretion curve starts to ascend and the amount filtered exceeds the amount reabsorbed.

142
Q

Substances that are reabsorbed using a Tm system

A

Glucose, amino acids, small peptides, myoglobin, ketones, calcium, phosphate.

143
Q

Characteristics of a gradient-time system

A

Carriers are not saturated, carriers have low affinity, high back leak

144
Q

Substances that are reabsorbed using a gradient-time system

A

Sodium, potassium, chloride and water

145
Q

Substances secreted using a Tm system

A

PAH. 20% filtered, 80% secreted.

146
Q

Graph for PAH secretion

A

At low plasma concentration secretion is 4 times the filtered load. When carriers become saturated, secretion reaches a plateau and the amount excreted is proportional to the amount filtered.

147
Q

How is the net transport rate for a substance calculated?

A

Net transport rate = filtered load - excretion rate = (GFR X Px) - (Ux X V)

148
Q

Effects of blood pressure changes in the kidney

A

GFR and RBF are maintained constant within the autoregulatory range. Urine flow is directly proportional to blood pressure due to pressure natriuresis and pressure diuresis.

149
Q

What is clearance and how is it calculated?

A

It’s the volume of plasma cleared of a substance over time. Clearance = excretion / Px = Ux X V / Px

150
Q

Characteristics of glucose clearance

A

At normal glucose levels, clearance is zero. Above treshold levels, clearance increases as plasma concentration increases but never reaches GFR as there’s always glucose reabsorption.

151
Q

Characteristics of inulin clearance

A

A constant amount of inulin is cleared regardless of plasma concentration (parallel line to x axis). Inulin clearance is equal to GFR because it’s not secreted nor reabsorbed. If GFR increases, clearance increases (line shifts upward), and vice versa.

152
Q

Characteristics of creatinine clearance

A

A constant amount of creatinine is cleared regardless of plasma concentration, but creatinine clearance is more than GFR because some is always secreted.

153
Q

Characterisics of PAH clearance

A

As plasma concentration increases, clearance decreases because carriers that mediate active secretion become saturated. At normal levels, PAH clearance = RPF because all is excreted.

154
Q

How is GFR calculated using inulin?

A

GFR is equal to inulin clearance because it’s only filtered and none is secreted nor reabsorbed. Cin = GFR = Uin X V / Pin

155
Q

How is creatinine production calculated?

A

Creatinine production = creatinine excretion = filtered load of creatinine = [Cr]p X GFR. Creatinine is filtered and secreted, not reabsorbed.

156
Q

How does inulin concentration change as it passes through the nephron?

A

Inulin becomes more concentrated as it passes through the tubules because water is being reabsorbed and not inulin.

157
Q

Gold standard to measure GFR

A

Inulin clearance because it’s filtered but not secreted nor reabsorbed.

158
Q

Gold standard to measure RPF

A

PAH clearance because some is filtered and the remaining is all secreted.

159
Q

How is effective RPF calculated?

A

PAH clearance = RPF = Upah X V / Ppah

160
Q

How is renal blood flow calculated?

A

ERPF / 1-Hct; ERPF = Upah X V / Ppah

161
Q

What does positive free water clearance mean?

A

Water is being eliminated. Hypotonic urine is being formed to increase plasma osmolarity.

162
Q

What does negative free water clearance mean?

A

Water is being conserved. Hypertonic urine is being formed to lower plasma osmolarity.

163
Q

How is free water clearance calculated?

A

V - (Uosm(V) / Posm)

164
Q

Which substance is cleared the most: PAH, inulin, glucose, creatinine

A

PAH

165
Q

Which substances are cleared more than glucose?

A

Sodium, inulin, creatinine, PAH

166
Q

Which substance is cleared the least: PAH, inulin, glucose, creatinine

A

Glucose

167
Q

Which substances are cleared more than inulin?

A

Creatinine, PAH

168
Q

Which substances are cleared less than creatinine?

A

Inulin, glucose, sodium

169
Q

Transporters in the luminal membrane of the proximal tubule

A

Secondary Na/glucose cotransporter, secondary Na/amino acid cotransporter, secondary Na/H countertransporter

170
Q

What substances are reabsorbed in the proximal tubule and how much?

A

Na (2/3 of filtered load), glucose (100%), amino acids (100%), HCO3 (indirectly, 80%), H20 (2/3), K (2/3), Cl (2/3)

171
Q

Tubular osmolarity at beginning and end of proximal tubule

A

At the beginning and end is isotonic with plasma but only 1/3 of the filtered load.

172
Q

Transporters in the basal membrane of proximal tubule

A

Na/K ATPase - luminal membrane secondary Na transporters depend on this.

173
Q

Transporters in the basolateral membrane of proximal tubule

A

Na/K ATPase - luminal membrane secondary Na transporters depend on this.

174
Q

Most energy-dependant process in the nephron

A

Active reabsorption of Na by the basal and basolateral Na/K ATPase

175
Q

Characteristics of the loop of henle

A

Descending limb is permeable to water so water difuses out and intraluminal osmolarity increases to 1,200mOsm Ascending limb is impermeable to water and Na is actively pumped out by Na/K/2Cl pump so fluid becomes hypotonic. Flow is slow, anything that increases flow, decreases capacity to concentrate urine.

176
Q

Characteristics of the collecting duct

A

Impermeable to water unless ADH is present. ADH increases permeability to H20 and urea to concentrate urine. Tight junctions with little back-leak.

177
Q

Specialized cells of the distal tubule and collecting duct

A

Principal cells (aldosterone) and intercalated cells (create HCO3)

178
Q

Actions of principal cells of the distal tubule and collecting duct

A

Aldosterone increases Na receptors in the membrane and increases primary transport by Na/K ATPase. Secondary transport of Na and secretion of K.

179
Q

Actions of the distal tubule and collecting duct

A

Reabsorption of Na and secretion of K (stimulated by aldosterone), acidification of the urine (secretion of H and creation of HCO3)

180
Q

Urine buffer systems

A

H2PO4- (dihydrogen phosphate) (tritratable acid) buffers 33% of secreted H. NH4+ (amonium) (nontritratable acid) buffers the remaining secreted H.

181
Q

How is potassium affected by acidosis?

A

High concentration of ECF H –> H diffuses to ICF –> K diffuses to ECF –> hyperkalemia

182
Q

How is potassium affected by alkalosis?

A

Low concentration of ECF H –> H diffuses to ECF –> K diffuses to ICF –> hypokalemia

183
Q

Potassium dynamics in acute alkalosis

A

Hypokalemia, ↑ intracellular K, ↑ renal K excretion, negative K balance

184
Q

Potassium dynamics in chronic alkalosis

A

Hypokalemia, ↓ intracellular K, ↑ renal K excretion, negative K balance

185
Q

Potassium dynamics in acute acidosis

A

Hyperkalemia, ↓ intracellular K, ↓ renal K excretion, positive K balance

186
Q

Potassium dynamics in chronic acidosis

A

Hyperkalemia, ↓ intracellular K, ↑ renal K excretion, negative K balance

187
Q

How is potassium balance in acute acidosis?

A

Positive (potassium is reabsorbed)

188
Q

How is potassium balance in acute alkalosis?

A

Negative (potassium is excreted)

189
Q

How is potassium balance in chronic alkalosis?

A

Negative (potassium is excreted)

190
Q

How is potassium balance in chronic acidosis?

A

Negative (potassium is excreted)

191
Q

How is plasma potassium concentration in alkalosis?

A

Hypokalemia

192
Q

How is plasma potassium concentration in acidosis?

A

Hyperkalemia

193
Q

What is the difference in potassium dynamics between acute and chronic alkalosis?

A

Acute alkalosis –> ↑ intracellular K; Chronic alkalosis –> ↓ intrecellular K

194
Q

What is the difference in potassium dynamics between acute and chronic acidosis?

A

Acute acidosis –> ↓ renal K excretion, positive K balance; Chronic acidosis –> ↑ renal K excretion, negative K balance

195
Q

Changes in respiratory acidosis

A

Hypoventilation –> ↑ PaCO2 –> ↑ H and slight ↑ in HCO3 –> ↓ pH

196
Q

Changes in respiratory alkalosis

A

Hyperventilation –> ↓ PaCO2 –> ↓ H and HCO3 –> ↑ pH

197
Q

Changes in metabolic acidosis

A

Gain of H or loss of HCO3 –> ↓ HCO3 –> ↑ pH. To see if gain of H or loss of HCO3 check anion gap.

198
Q

Changes in metabolic alkalosis

A

Loss of H or gain in HCO3 –> ↑ HCO3 –> ↑ pH. To see if gain of H or loss of HCO3 check anion gap.

199
Q

Normal values of PCO2, HCO3 and pH

A

pH = 7.4; PCO2 = 40mmHg; HCO3 = 24mmol/L

200
Q

↑pH, ↑ HCO3, ↑PCO2, ↓PO2, alkaline urine

A

Partially compensated metabolic alkalosis

201
Q

↓pH, ↑PCO2, ↑HCO3, ↓PO2, acid urine

A

Partially compensated respiratory acidosis

202
Q

↑pH, ↓PCO2, ↓HCO3, normal PO2, alkaline urine

A

Partially compensated respiratory alkalosis

203
Q

↓pH, ↓PCO2, ↓HCO3, normal PO2, acid urine

A

Partially compensated metabolic acidosis

204
Q

Normal plasma anion gap value

A

PAG = 12

205
Q

Conditions that increase plasma anion gap

A

Lactic acidosis, ketoacidosis, ingestion of salicylate

206
Q

Hyperchloremic non-anion gap metabolic acidosis

A

Loss of HCO3 (as in diarrhea) causes increased absorption of solutes and water, increasing Cl. Therefore ↓HCO3 and ↑Cl with a plasma anion gap of 12.

207
Q

Factors that affect hormone binding protein synthesis

A

Estrogen increases binding proteins; androgens decrease binding proteins. In pregnancy there’s increased total hormones with normal levels of free hormone.

208
Q

Site of synthesis of CRH

A

Paraventricular nucleus

209
Q

Site of synthesis of TRH

A

Paraventricular nucleus

210
Q

Site of synthesis of PIF

A

Arcuate nucleus

211
Q

Site of synthesis of GHRH

A

Arcuate nucleus

212
Q

Site of synthesis of GnRH

A

Preoptic region

213
Q

Site of synthesis of ADH

A

Supraoptic and paraventricular nuclei

214
Q

How do hypothalamic hormones reach the anterior pituitary?

A

Hormones are released in the hypophyseal-portal system

215
Q

Hypothalamic hormones

A

GHRH, GnRH, PIF (dopamine), TRH, CRH, Somatostatin, ADH, prolactin

216
Q

Anterior pituitary hormones

A

ACTH, TSH, LH, FSH, GH, prolactin

217
Q

Sheehan syndrome

A

Ischemic necrosis of the pituitary due to severe blood loss during delivery. Causes hypopituitarism.

218
Q

Obstruction of pituitary stalk

A

Adenoma compresses pituitary stalk and decreases secretion of anterior pituitary hormones except prolactin.

219
Q

What prevents downregulation of pituitary receptors?

A

Pulsatile release of hypothalamic hormones.

220
Q

Hyperprolactinemia

A

Results from dopamine antagonists or pituitary adenomas that compress the pituitary stalk. Amenorrhea, galactorrhea, decreased libido, impotence, hypogonadism

221
Q

What hormone controls release of cortisol and adrenal androgens?

A

ACTH

222
Q

What hormone regulates release of aldosterone?

A

Angiotensin II and also potassium in hyperkalemia

223
Q

Layers of the adrenal cortex

A

From external to internal: glomerulosa (aldosterone), fasciculata (cortisol), reticularis (androgens). “Salt, Sugar and Sex; the deeper it goes the sweeter it gets”

224
Q

Consequences of loss of zona glomerulosa

A

No aldosterone: loss of Na, ↓ECF, ↓blood pressure, circulatory shock, death

225
Q

Consequences of loss of zona reticularis

A

No cortisol: circulatory failure (cortisol is permissive for cathecolamine vasoconstriction), can’t mobilize energy stores during exercise of cold (hypoglycemia)

226
Q

Consequences of loss of adrenal medulla

A

No epinephrine: decreased capacity to mobilize fat and glycogen during stress. Not necessary for survival.

227
Q

What are the 17-OH steroids?

A

17OHpregnenolone, 17OHprogesterone, 11-deoxycortisol, cortisol. Urinary 17OH steroids are an index of cortisol secretion.

228
Q

What is the rate-limiting enzyme for steroid hormone synthesis?

A

Desmolase - converts cholesterol into pregnenolone

229
Q

What are the 17-ketosteroids?

A

DHEA and androstenidione

230
Q

DHEA

A

Weak androgen 17-ketosteroid conjugated with sulfate to make it water-soluble

231
Q

What is measured as an index of androgen production?

A

Urinary 17-ketosteroids. In females and prepubertal males is an index of adrenal 17-ketosteroids. In postpubertal males is an index of 2/3 adrenal androgens and 1/3 testicular androgens.

232
Q

Stimulus for the zona glomerulosa

A

Angiotensin II and potassium in hypekalemia stimulate production of aldosterone

233
Q

Hormone responsible for negative feedback for ACTH release

A

Cortisol

234
Q

Enzyme deficiencies that produce congenital adrenal hyperplasia and low cortisol levels

A

21β-OH, 11β-OH and 17α-OH all result in low cortisol levels.

235
Q

21β-OH deficiency

A

No aldosterone: loss of Na, ↓ECF, ↓blood pressure in spite of high renin and angiotensin II, circulatory shock, death. No cortisol (low 17OH steroids): skin hyperpigmentation (due to excess ACTH), adrenal hyperplasia, hypotension (persmissive for catecholamines), fasting hypoglycemia. Excess androgens (17-ketosteroids): female pseudohermaphrodite, hirsutism

236
Q

11β-OH deficiency

A

Excess 11-deoxycorticosterone: Na and water retention, low-renin hypertension. No cortisol (low 17OH steroids): skin hyperpigmentation (due to excess ACTH), adrenal hyperplasia, fasting hypoglycemia. Excess androgens (17-ketosteroids): female pseudohermaphrodite, hirsutism

237
Q

17α-OH deficiency

A

Excess 11-deoxycorticosterone and low aldosterone (no AII): Na and water retention, low-renin hypertension. No cortisol: skin hyperpigmentation (due to excess ACTH), adrenal hyperplasia; corticosterone partially compensates low cortisol levels. No 17-ketosteroids: male pseudohermaphrodite, no testosterone, no estrogen.

238
Q

↓17OH-steroids ↑ACTH, ↓blood pressure, ↓mineralocorticoids, ↑17-ketosteroids

A

21β-OH deficiency

239
Q

↓17OH-steroids ↑ACTH, ↑blood pressure, ↓aldosterone, ↑11-deoxycorticosterone, ↑17-ketosteroids

A

11β-OH deficiency

240
Q

↓17OH-steroids ↑ACTH, ↑blood pressure, ↑ aldosterone, ↑11-deoxycorticosterone, ↓17-ketosteroids

A

17α-OH deficiency

241
Q

Stress hormones

A

GH, Glucagon, cortisol, epinephrine

242
Q

Actions of GH in stress situations

A

Mobilizes fatty acids by increasing lipolysis in adipose tissue

243
Q

Actions of glucagon in stress situations

A

Mobilizes glucose by increasing liver glycogenolysis

244
Q

Actions of cortisol in stress situations

A

Mobilizes fat, carbs and proteins

245
Q

Actions of epinephrine in stress

A

Mobilizes glucose via glycogenolysis and fat via lipolysis.

246
Q

Metabolic actions of cortisol

A

1) Protein catabolism and delivery of amino acids; 2) lipolysis and delivery ofr fatty acids and glycerol 3) gluconeogenesis raises glycemia; also inhibits glucose uptake.

247
Q

Permissive actions of cortisol

A

Enhances glucagon (without cortisol –> fasting hypoglycemia); enhances epinephrine (without cortisol –>hypotension)

248
Q

α-MSH

A

Stimulates melanocytes and causes darkening of skin. Synthesized along with ACTH from pro-opiomelanocortin.

249
Q

↑cortisol, ↓CRH, ↓ACTH, no hyperpigmentation

A

Primary hypercortisolism

250
Q

↓cortisol, ↑CRH, ↑ACTH, hyperpigmentation

A

Addison disease - primary hypocortisolism

251
Q

↑cortisol, ↓CRH, ↑ACTH, hyperpigmentation

A

Secondary hypercortisolism

252
Q

↓cortisol, ↑CRH, ↓ACTH, no hyperpigmentation

A

Secondary hypocortisolism

253
Q

↓cortisol, ↓CRH, ↓ACTH, no hyperpigmentation, symptoms of excess cortisol

A

Steroid administration

254
Q

Cushing syndrome

A

Protein depletion, weak inflammatory response, poor wound healing, hyperglycemia, hyperinsulinemia, insulin resistance, hyperlipidemia, osteoporosis, purple striae, hirsutism, hypertension, hypokalemic alkalosis, buffalo hump

255
Q

Actions of aldosterone

A

↑Na channels in lumen of principal cells, ↑activity of Na/K ATPase of principal cells –> increases Na reabsorption. Also ↑ secretion of K and H leading to hypokalemic metabolic alkalosis.

256
Q

Addison disease

A

↑ ACTH, hyperpigmentation, hypotension (no aldosterone, no cortisol), hyperkalemic metabolic acidosis (no aldosterone), loss of body hair (no androgens), hypoglycemia, ↑ ADH secretion

257
Q

Causes of secondary hyperaldosteronism

A

CHF, vena cava constriction, cirrhosis, renal artery stenosis

258
Q

Primary hyperaldosteronism

A

Na and water retention, hypertension, hypokalemic metabolic alkalosis, ↓ renin and angiotensin, no edema due to pressure diuresis and natriuresis.

259
Q

Primary hypoaldosteronism

A

Na and water loss, hypotension, hyperkalemic metabolic acidosis, ↑ renin and angiotensin II, no edema

260
Q

Secondary hyperaldosteronism

A

↑ renin and angiotensin II, ↑ Na and water retention in venous circulation, edema

261
Q

Factors that influence ADH secretion

A

↑ osmolarity –> ↑ ADH secretion; ↓ blood volume –> baroreceptors –> medulla –> ↑ ADH secretion

262
Q

Actions of ADH

A

Inserts water channels in luminal membrane of collecting ducts, increases reabsorption of water.

263
Q

Central diabetes insipidus

A

Not enough ADH secreted. Dilute urine is formed in spite of water deprivation. Responds to injected ADH.

264
Q

Nephrogenic diabetes insipidus

A

ADH is secreted but ducts are unresponsive to it. Dilute urine is formed in spite of water deprivation or injected ADH.

265
Q

SIADH

A

Excessive secretion of ADH in spite of low osmolarity. Concentrated urine is formed.

266
Q

↓ permeability of collecting ducts, ↑ urine, ↓ urine osmolarity, ↓ ECF, ↑ osmolarity

A

Diabetes insipidus

267
Q

↑ permeability of collecting ducts, ↓ urine, ↑ urine osmolarity, ↓ ECF, ↑ osmolarity

A

Dehydration

268
Q

↑ permeability of collecting ducts, ↓ urine, ↑ urine osmolarity, ↑ ECF, ↓ osmolarity

A

SIADH

269
Q

↓ permeability of collecting ducts, ↑ urine, ↓ urine osmolarity, ↑ ECF, ↓ osmolarity

A

Primary polydipsia

270
Q

Actions of ANP

A

Atrial stretch or ↑ osmolarity –> ANP secretion –> dilation of afferent, constriction of efferent –> ↑ GFR –> natriuresis; also decreases permeability of collecting ducts to water.

271
Q

Delta cells of the pancreas

A

Between alpha and beta cells, represent 5% of islets. Secrete somatostatin.

272
Q

Alpha cells of the pancreas

A

Near the periphery of the islets, represent 20%. Secrete glucagon.

273
Q

Beta cells of the pancreas

A

In the center of the islets, represent 60-75%. Secrete insulin and C peptide.

274
Q

Insulin receptor

A

Has intrinsic tyrosine kinase activity. Insulin receptor substrate binds tyrosine kinase, activates SH2 domain proteins: PI-3 kinase (translocation of GLUT-4), p21RAS.

275
Q

Tissues that require insulin for glucose uptake

A

Resting skeletal muscle and adipose tissue

276
Q

Tissues independent of insulin for glucose uptake

A

Brain, kidneys, intestinal mucosa, red blood cells, beta cells of the pancreas.

277
Q

Anabolic hormones

A

Insulin, GH/IGF-1, androgens, T3/T4, IGF-1 (somatomedin C)

278
Q

Effects of insulin on potassium

A

Increases Na/K ATPase uptake of K. Insulin + glucose used to treat hyperkalemia.

279
Q

Mechanism of insulin release

A

Glucose enters β cells and is metabolized –> ↑ ATP –> closes K channels –> ↑ depolarization –> ↑ Ca influx –> exocytosis of insulin.

280
Q

Factors that stimulate secretion of insulin

A

Glucose, arginine, GIP, glucagon

281
Q

Factors that inhibit insulin release

A

Somatostatin, norepinephrine via α1 receptors

282
Q

↑ glucose, ↑ insulin, ↑ C peptide

A

Type 2 diabetes

283
Q

↑ glucose, ↓ insulin, ↓ C peptide

A

Type 1 diabetes

284
Q

↓ glucose, ↑ insulin, ↑ C peptide

A

Insulinoma

285
Q

↓ glucose, ↑ insulin, ↓ C peptide

A

Factitious hypoglycemia (insulin injection)

286
Q

Actions of somatomedin C

A

Increases cartilage synthesis at epiphyseal plates (↑ bone length). Also ↑ lean body mass. Protein-bound and long half-life correlates to GH secretion. Also called IGF-1.

287
Q

Secretion of GH

A

Pulsatile during non-REM sleep; more frequent in puberty due to increased androgens; requires thyroid hormones; decreases in the elderly.

288
Q

Factors that stimulate GH secretion

A

Deep sleep, hypoglycemia, exercise, arginine, GHRH, low somatostatin

289
Q

Factors that inhibit GH secretion

A

Negative feedback by GH on GHRH; positive feedback on somatostatin by IGF-1

290
Q

Dwarfism

A

Due to GH insensitivity during prepuberty

291
Q

Acromegaly

A

Due to excess GH in postpuberty. Enlargement of hands, feet and lower jaw, increased proteins, decreased fat, visceromegaly, cardiac insuficiency.

292
Q

Composition of bone

A

Phosphate and calcium precipitate forming hydroxyapatite in osteoid matrix.

293
Q

Actions of PTH

A

Rapid actions: increases Ca reabsorption in distal tubules and decreases phosphate reabsorption in proximal tubules, thus lowering blood phosphate and lowering solubility product which leads to bone resorption and raises plasma Ca. Slow actions: increases number and activity of osteoclasts (via osteoclast activating factor released by osteoblasts), increases activity of alpha-1 hydroxylase in the proximal tubules which increases active vitamin D and absorption of Ca and phosphate in the instetines.

294
Q

Clinical features of primary hyperparathyroidism

A

↑ plasma Ca and ↓ plasma phosphate, phosphaturia, polyuria, calciuria (filtered load of Ca exceeds Tm), ↑ serum alkaline phosphatase, ↑ urinary hydroxyproline, muscle weakness, easy fatigability.

295
Q

Clinical features of primary hypoparathyroidism

A

↓ plasma Ca and ↑ plasma phosphate, hypocalcemic tetany due to increased excitability of motor neurons.

296
Q

↑ PTH, ↑ Ca, ↓ phosphate

A

Primary hyperparathyroidism. Causes: parathyroid adenoma (MEN I and II), ectopic PTH tumor (lung squamous CA)

297
Q

↓ PTH, ↓ Ca, ↑ phosphate

A

Primary hypoparathyroidism. Cause: surgical removal of parathyroid.

298
Q

↑ PTH, ↓ Ca, ↑ phosphate

A

Secondary hypoparathyroidism due to renal failure (no active vitamin D, decreased GFR)

299
Q

↑ PTH, ↓ Ca, ↓ phosphate

A

Secondary hyperparathyroidism. Causes: deficiency of vitamin D due to bad diet or fat malabsorption.

300
Q

↓ PTH, ↑ Ca, ↑ phosphate

A

Secondary hypoparathyroidism due to excess vitamin D.

301
Q

Vitamin D synthesis

A

Dietary and skin cholecalciferol is hydroxylated by 25-hydroxylase in the liver and activated to 1,25 di-OH cholecalciferol by 1-alpha hydroxylase in the proximal tubules.

302
Q

Actions of 1,25 di-OH cholecalciferol

A

Increases Ca binding proteins by intestinal cells which increases intestinal reabsorption of Ca and phosphate. Also increases reabsorption of Ca in the distal tubules. Increased serum Ca promotes bone deposition.

303
Q

Osteomalacia

A

Underminerilized bone in adults due to vitamin D deficiency leads to bone deformation and fractures. Low calcium leads to secondary hyperparathyroidism.

304
Q

Rickets

A

Underminerilized bone in children due to vitamin D deficiency leads to bone deformation and fractures. Low calcium leads to secondary hyperparathyroidism.

305
Q

Excess vitamin D

A

Leads to bone reosprtion and demineralization

306
Q

Synthesis of thyroid hormones

A

1) Iodine is actively transported into follicle cell; 2) thyroglobulin is synthesized in the RER, glycosylated in the SER and packaged in the GA; 3) Peroxidase is found in the luminal membrane and catalizes oxidation of I-, iodination of thyroglobulin and coupling to form MITs and DITs; 4) iodinated thyroglobulin is stored in the follicle lumen.

307
Q

Structure of thyroid hormones

A

T4 has iodine attached to carbons 3 and 5 of both fenol rings; T3 has iodide attached to carbons 3 and 5 of the amino terminal fenol ring and the 3 prime carbon of the hydroxyl end fenol ring; reverse T3 has iodide in carbon 3 of the amino terminal fenol ring but not carbon 5.

308
Q

Secretion of thyroid hormones

A

Iodinated thyroglobulin is endocytosed from the lumen of the follicles into lysosomes. Thyroglobulin is degraded into amino acids, T3, T4, DITs and MITs. T4 and T3 are secreted in a 20:1 ratio. DITs and MITs are deiodinated and iodine is recycled.

309
Q

Transport of thyroid hormones

A

99% is bound to TBG, 1% is free. T4 has greater affinity for TBG and a half-life of 6 days. T3 has greater affinity for nuclear receptor and is the active form with a 1 day half-life. 50:1 T4/T3 ratio in periphery.

310
Q

Activation and degradation of thyroid hormones

A

5’ monodeiodinase activates T4 into T3. 5-monodeiodinase inactivates T4 into reverse T3.

311
Q

Actions of thyroid hormones

A

↑ metabolic rate by ↑ Na/K ATPase except in brain, uterus and testes; essential for brain maturation and menstrual cycle; permissive for bone growth; permissive for GH synthesis and secretion; ↑ clearance of cholesterol; required for activation of carotene; ↑ intestinal glucose absorption; ↑ affinity and number of β1 receptros in the heart.

312
Q

Effects of hypothyroidism in newborns

A

↓ dendritic branching and myelination lead to mental retardation.

313
Q

Effects of hypothyroidism in juveniles

A

Cretinism results in ↓ bone growth and ossification –> dwarfism. Due to lack of permissive action on GH.

314
Q

Control of thyroid hormone secretion

A

Circulating T4 is responsible for negative feedback of TSH by decreasing sensitivity to TRH. T4 is converted to T3 in the thyrotroph to induce negative feedback.

315
Q

Effects of TSH

A

Rapid actions: ↑ iodide trapping, ↑ synthesis of thyroglobulin, ↑ reuptake of iodinated thyroglobulin, ↑ secretion of T4; late effects: ↑ blood flow to thyroid gland, ↑ hypertrophy of follicles and goiter.

316
Q

↓ T4, ↑ TSH, ↑ TRH

A

Primary hypothyroidism; ↑ TSH is the more sensible index

317
Q

↓ T4, ↓ TSH, ↑ TRH

A

Pituitary (secondary) hypothyroidism

318
Q

↓ T4, ↓ TSH, ↓ TRH

A

Hypothalamic (tertiary) hypothyroidism

319
Q

↑ T4, ↑ TSH, ↓ TRH

A

Pituitary (secondary) hyperthyroidism

320
Q

↑ T4, ↓ TSH, ↓ TRH

A

Graves disease

321
Q

Pathophysiology of iodine deficiency

A

Thyroid makes less T4 and more T3 so actions of T3 may be normal but low levels of T4 stimulate TSH secretion with development of goiter. Thus euthyroid with goiter.

322
Q

Clinical features of hypothyroidism

A

↓ basal metabolic rate with cold intolerance, ↓ cognition, hyperlipidemia, nonpitting myxedema (mucopolysacchride accumulation around eyes retains water), physiologic jaundice (↑ carotene), hoarse voice, constipation, anemia, lethargy

323
Q

Clinical features of hyperthyroidism

A

↑ metabolic rate with heat intolerance and sweating, ↑ apetite with weight loss, muscle weakness, tremor, irritability, tachycardia, exophthalmos.

324
Q

Leydig cells

A

Stimulated by LH; produce testosterone for peripheral tissues and Sertoli cells. Testosterone provides negative feedback for LH secretion by pituitary.

325
Q

Sertoli cells

A

Stimulated by FSH; produce inhibins (inhibits secretion of FSH), estradiol (testosterone is converted by aromatase), androgen binding proteins and growth factors for sperm. Responsible for development of sperm in males. Also MIH in male fetus.

326
Q

↓ sex steroids, ↑ LH, ↑ FSH

A

Primary hypogonadism or postmenopause.

327
Q

↓ sex steroids, ↓ LH, ↓ FSH

A

Pituitary hypogonadism or constant GnRH infusion (downregulates GnRH receptors of pituitary.

328
Q

↑ sex steroids, ↓ LH, ↓ FSH

A

Anabolic steroid therapy. LH supression causes Leydig cell atrophy with decreased Leydig testosterone which suppresses spermatogenesis.

329
Q

↑ sex steroids, ↑ LH, ↑ FSH

A

Pulsatile infusion of GnRH

330
Q

Fetal development of male structures

A

LH –> Leydig cells –> testosterone –> Wolffian ducts (internal male structures: epididymis, vasa deferentia ans seminal vesicles). Testosterone + 5-alpha reductase –> dihydrotestosterone –> urogenital sinus and external organs. MIH by Sertoli cells –> regression of Mullerian ducts and female structures.

Step 1 Complete (29 decks)

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