This is a review for the USMLE Step 1 of Physiology. It contains anything you need to know for your exam in pictures, diagrams and tables.

2. 𝑉 =
𝐴
𝐶
𝑂𝑆𝑀 = 2 𝑁𝑎 +
𝐵𝑈𝑁
2.8
+
𝐺𝑙𝑢𝑐𝑜𝑠𝑒
18
𝑄𝑓 = 𝑘 𝑃 𝑐 + 𝜋𝑖𝑓 − (𝑃𝑖𝑓 + 𝜋 𝑐)
𝐵𝑙𝑜𝑜𝑑 𝑉𝑜𝑙𝑢𝑚𝑒 =
𝑃𝑙𝑎𝑠𝑚𝑎 𝑉𝑜𝑙𝑢𝑚𝑒
1 − 𝐻𝑒𝑚𝑎𝑡𝑜𝑐𝑟𝑖𝑡
∆𝑃 = 𝑃1 − 𝑃2
P1= Upstream pressure
P2= Pressure at the end
𝑄 =
∆𝑃
𝑅𝑒𝑠𝑖𝑠𝑡.
Q= Flow
∆𝑃= Pressure Gradient
𝑆𝑉 = 𝐸𝐷𝑉 − 𝐸𝑆𝑉
EDV= End diastolic volume
ESV= End systolic volume
𝑅𝑒𝑦𝑛𝑜𝑙𝑑′
𝑠 # =
(𝐷𝑖𝑎𝑚𝑒𝑡𝑒𝑟)(𝑉𝑒𝑙)(𝐷𝑒𝑛𝑠𝑖𝑡𝑦)
𝑉𝑖𝑠𝑐𝑜𝑠𝑖𝑡𝑦
>2000 = Turbulent flow
<2000 = Laminar flow
𝑅𝑒𝑠𝑖𝑠𝑡𝑎𝑛𝑐𝑒 =
𝑣𝐿
𝑟4
V= Viscosity
R= Radius 50% = 16x
𝐶𝑂 =
𝑀𝐴𝑃
𝑇𝑃𝑅
MAP= Mean arterial pressure
TPR= Total Peripheral Resistance
𝐶 =
∆𝑉
∆𝑃
C = Compliance
∆ = Change
veins
arteries

3. 𝐹𝑙𝑜𝑤 =
𝑂𝑥𝑦𝑔𝑒𝑛 𝑈𝑝𝑡𝑎𝑘𝑒
𝐴𝑟𝑡𝑒𝑟𝑦 𝑂2 − 𝑉𝑒𝑖𝑛 𝑂2
Blood flow in an organ
𝐶𝑎𝑟𝑑𝑖𝑎𝑐 𝐼𝑛𝑑𝑒𝑥 =
𝐶𝑂
𝐵𝑆𝐴
BSA= Body Surface Area
𝑉 𝐸 = 𝑉𝑇 × 𝑓
VE= Total Ventilation
VT= Tidal volume
F= Respiratory rate
𝑉 𝐴 = 𝑉 𝑇 − 𝑉𝐷 𝑓
VA= Alveolar ventilation
VD= Dead space
𝑃𝐼𝑂2 = (𝑃𝑎𝑡𝑚 − 𝑃𝐻2 𝑂)𝑓𝑂2
PIO2 = Partial pressure of inspired gas
PH2O = Partial pressure of H2O vapor (47)
47
𝐷𝑖𝑓𝑓𝑢𝑠𝑖𝑜𝑛 =
𝑆𝐴 × ∆𝑃 × 𝑆𝑜𝑙
𝑇√𝑚𝑊
SA = Surface Area
Sol = Solubility
T= Membrane thickness
mW= Molecular weight
𝑃 𝐴 𝐶𝑂2 =
𝑀𝑒𝑡𝑎𝑏𝑜𝑙𝑖𝑠𝑚
𝐴. 𝑉𝑒𝑛𝑡𝑖𝑙𝑎𝑡𝑖𝑜𝑛
𝑃 𝐴 𝑂2 = 𝑃𝑎𝑡𝑚 − 47 𝑓𝑂2 −
𝑃𝐶𝑂2
𝑅
Patm= Atmospheric pressure
f= fraction of Oxygen in the air (21%)
R= Gas constant (0.8-1)
𝐹𝐹 =
𝐺𝐹𝑅
𝑅𝑃𝐹
FF= Filtration fraction
GFR= Glomerular Filtrat.
RPR= Renal Plasma Flow
600
12020%
𝐹𝑖𝑙𝑡𝑒𝑟𝑒𝑑 𝐿𝑜𝑎𝑑 = 𝐺𝐹𝑅 × 𝑃𝑥
Px = Free concentration of substance
in plasma

4. Concentration of Solute
VolumeVolume
HYPO-osmolar
HYPER-osmolar
ECFICF Plasma
300 mOsm/L 300 mOsm/L
Cell Dehydration

5. Loss of Isotonic Fluid
Hemorrhage
Loss of Hypotonic Fluid
Diabetes Insipidus, Sweating or Dehydration
Gain of Isotonic Fluid Gain of Hypotonic Fluid
Gain of Hypertonic FluidLoss of Hypertonic Fluid
Adrenal Insufficiency

6. FILTRATION
Hydrostatic Pressure Pc = CAPILLARY push out
Oncotic force π = INTERSTITIUM pull out
ABSORPTION
Oncotic force π = CAPILLARY pull IN
Hydrostatic Pressure Pc= INTERSTITIUM push IN
Capillary
Interstitium
Interstitium
𝑄𝑓 = 𝑘 𝑃 𝑐 + 𝜋𝑖𝑓 − (𝑃𝑖𝑓 + 𝜋 𝑐)
Forces of Filtration
-Hydrostatic pressure If is opposing filtration

7. V
Pc
Increased blood flow, venous pressure
Elevated blood volume, Left ventricle failure
Pulmonary edema –Wedge up (cardiogenic)
πif
Thyroid dysfunction
Fluid accumulation
Non-pitting edema
πc
Liver failure (Cirrhosis)
Nephrotic syndrome
Congestive Heart Failure
K (capillary permeability)
Circulating agents, eg.
TNF-alpha, bradykinin, histamine, cytokines
Increase fluid filtration - edema
𝑉 =
𝐴
𝐶
𝑉 =
300𝑚𝑔
0.05
𝑚𝑔
𝑚𝑙
= 6000 𝑚𝑙
TRACERS
Plasma: Albumin
ECF: Inulin
Total body water: Urea

8. • Follow the concentration
gradient.
• Continuous.
• Not affected by action
potential.
• ALWAYS open (K+)
• Depends on + or – charges
• Creates and affected by action
potential.
• Create concentration
differences.
• FAST (Na+) Closed at rest
• SLOW (K+ and Ca++)
• Protein transporter
• Neuromuscular junction Ca+
• It’ll take an electrical stimulus
and turn it into a chemical
stimulus.
Ungated

9. Low Cl-
High K+
Low Na+
-90mV
High Cl-
Low K+
High Na+
Na
K
ATP

10. Depolarization: Rapid flux of Na+ into the cell
Repolarization: Na+/K+ ATPase pump
Hyperpolarization: K+ leaves the cell, becomes more negative
2- Absolute Refractory Period –
NOTHING will incite a response
4- Relative Refractory Period –
needs GREATER than normal
stimulus
Na+ channels close

11. SA node Action Potential
4 4
0
3
OR Slow influx of Ca+

12. +
-
In
Out
Out
-90mV
In

13. 25mm/sec
P
Q
R
S
T
PR
QRS
QT
ST
T
Atrium Depolarization
Ventricular Depolarization
Repolarization
SA to AV
0.12 sec
0.35-0.44 - Arrythmias
Phase 0 Phase 3
200 ms
300
150
100
75
60
50
40
40 ms

14. Lead-AVF
Lead-I Lead+I
Lead+AVF
Lead-AVF
Lead-I Lead+I
Lead+AVF
Lead-AVF
Lead-I Lead+I
Lead+AVF
Lead-AVF
Lead-I Lead+I
Lead+AVF
Voltages:
Lead +I
Lead +AVF
Normal axis
Voltages:
Lead +I
Lead -AVF
Left axis
Voltages:
Lead -I
Lead +AVF
Right axis
Extreme
right axis
Left axis
deviation
Right axis
deviation Normal

15. PR progressively lengthens and drops
PR Drops all of a sudden
Atrium (60-100) and Ventricle (30-40) have a complete
dissociation, beat independently. Bradycardia

16. Myosin
Actin Actin

17. Determined by Venous return
and End Diastolic Volume
120 ml of Blood = Optimally filled

18. X
Ventricular Preload
SystolicPerformance
C
A
N
B
E
D F
IVIII
Decreases preload
and performance
- Preload but +
performance =
+ contractility
All points in the
same line (D, C, E)
have the same
contractility
Increase contractility
Decrease contractility
On different lines
CO = Preload +
Contractility
+ Preload and +
performance =
- contractility.

19. Heart
Dysfunction
Diastolic
Filling
dysfunction
(Venous return)
Hemorrhage
Preload defects
Hypertrophic
Restrictive
Systolic
Pressure factors
Increased TPR
Increased
afterload
Hypertension
= Concentric
Hypertrophy
Obstruction
Aortic Stenosis
Volume factors
Increased End
Diastolic Volume
Aortic
insufficiency
Mitral
insufficiency
Eccentric
Hypertrophy
Increased
backflow

20. Facilitate
exchange

21. Pulmonary circuit has a
high compliance and
low resistance.
CO %
Lungs: 100%
Liver: 25%
Kidneys: 20%
Brain: 15%
Heart: 5%
Cardiac AV difference
is very large = Large
extraction.

22. Flow equal at ALL points.
Total resistance is equal to the SUM.
Adding resistances will increase the total.
Within organs
Flow is independent from each other
NOT equal at all times, it varies.
There is no summation of resistances.
Total is always LESS than any of the resistances
Between organs (if subtracts one, R increases)
1
𝑅𝑇
=
1
𝑅1
+
1
𝑅2
+
1
𝑅3
𝑅𝑇 = 𝑅1 + 𝑅2 + 𝑅3

23. Pulse Pressure
Systolic
Cardiac Output
Heart Rate
Stroke volume
Compliance
Diastolic
TPR
Radius
Compliance
ACEIs
Alpha blocker
Calcium channel blocker
Increases as you go DISTALLY
from the heart.

24. Intrinsic Regulation - Metabolites
Coronary Circulation
Adenosine
Vasodilates
Cerebral Circulation
Pa Co2
Exercising Skeletal
Muscle
Lactic Acid - Vasodilates
Systolic Diastolic MAP
Kidneys
Under normal
circumstances.
Eg. Hemorrhage

25. Extrinsic Regulation
SkinResting Muscle
CNS – alpha receptors
Other – Angiotensin and Beta 2

26. 80%
67%
26%
26%
40%
65%
50%
60%

27. System Blood
flow
MAP TPR Blood
volume
# Perfused
capillary
Capillary
surface
area
PO2 PCO2 Temp pH Preload
Pulmonary
Circuit Gas
exchange
Arterial
system
Severe
Venous
system
Exercising
muscle
Filtration Pressure
Skin
Coronary /
Heart
Severe
Cerebral
Renal and
GI

28. Normal
Pressure tracing 80
Diastole
(V Filling)
Systole
S1
S2
15

29. EKG Event Valve Sound Sound abnormality
P Atrial depolarization Mitral Opening S3 and S4
S3 – Volume overload
S4 – Stiff ventricle
QRS
Ventricular
depolarization
Mitral Closure S1
PR interval AV node conduction None None
T wave
Ventricular
repolarization
Aortic Valve
(1st),
Pulmonary
valve closure
(2nd)
S2
Widening – Pulmonic
stenosis, Right bundle
branch block.
Fixed – ASD, L-R shunt
Paradoxical – Left Bundle
branch block, Aortic
stenosis.
ST interval Ejection phase Aortic Opening None

30. . A P . 2-3rd
5-6th
.
Aortic
Pulmonary
Tricuspid
Mitral
Close at beginning of S
Open at beginning of D
Close at beginning of D
Open at beginning of S
Sounds are generated at the time of closure.
S1 beginning of systole
S2 beginning of diastole
Stenosis – Anterograde Insufficiency – Retrograde
MT
A: Systolic – Aortic stenosis
P: Systolic – Mitral insufficiency
T: Systolic – Tricuspid insufficiency
T: Diastolic – Tricuspid stenosis
M: Diastolic – Mitral stenosis and aortic insufficiency
T
P

31. Murmur
Systolic
Patent Ductus
arteriosus
Holosystolic
Machine like
murmur
Bicuspid aortic
valve
Early systolic
High-frequency
click
Right 2nd
interspace
Hypertrophic
Cardiomyopathy
Crescendo-
decrescendo
murmur
Between apex and
left sternal
Radiates to the
suprasternal
notch
Louder standing
up
Aortic Stenosis
Early Systolic Click,
ejection
Crescendo-
decrescendo
murmur
Pulse late and
weak
Old age /
Rheumatic F.
Congenital
Bicuspid valve
Angina, syncope,
CHF
Pulmonary
Stenosis
Tetralogy of Fallot
Harsh ejection
murmur
Systolic thrill
Mitral
Regurgitation
Pansystolic
blowing
Louder w/
squatting
Radiates to axilla
Increases After
load
Acute Rheumatic
Fever
MV Prolapse
complication
Libman-Sacks
endocarditis
Mitral Valve
Prolapse
Myxoid
degeneration
Late-systolic Click
Marfan syndrome
Ehlers-Danlos
Decreases
w/squatting
Tricuspid
Regurgitation
Pansystolic
Increase right
heart Flow
Taking a Deep
breath
IV drug users w/
endocarditis
Dilated
cardiomyopathy
Septal Defects
Ventricular
Harsh Holosystolic
Atrial
Fixed Splitting of
S2 (Aortic and
Pulmonary
closure)
Diastolic
Aortic
Regurgitation
Blowing murmur
Widened pulse
pressure
Aortic root
dilation
Infectious
Endocarditis
Aortic root
aneurysm
Decreases in
intensity
Pulmonary
Regurgitation
Mitral Stenosis
Opening snap
Chronic
Rheumatic Fever
Diastolic Rumble
Mid-late murmur
Gradual decrease
in mid-late
Tricuspid Stenosis
Mid-late murmur

32. A: Right atrial contraction - depolarization
C: Bulging of tricuspid valve during right ventricular contraction (uncommon)
X: Right atrial relaxation (filling)
V: Inflow of venous blood into the atrium during ventricular systole.
Y: Filling of the right ventricle, after opening the tricuspid.
Jugular Venous Tracing

33. Normal Tracing Atrial Fibrillation
Tricuspid Insufficiency Tricuspid Stenosis
Loss of x descent – Not enough time for veins to empty
Blood backs up into the RA, increases pressure. Loss of x descent – Pressure in the atrium will increase

34. Volume
Pressure
Ejection
Isovolumetric
ContractionIsovolumetric
relaxation
Filling
Aortic valve
closes
Aortic valve
opens
Mitral valve
opens
Mitral valve
closes
Stroke Volume
ESV EDV
Pressure Volume Loops
Aortic Insufficiency: Increased
preload, increased SV, increased
pressure.
Systolic Heart Failure: Increased
preload, decreased pressure.
Essential Hypertension: Increased
pressure, little change in preload.
Increased Contractility: Decreased
preload, increased ejection fraction,
increased pressure.
Exercise: Increased preload, increased
ejection fraction, increased pressure.
Preload
Afterload
Aortic Stenosis: Increased afterload,
little increase in EDV, increased
pressure, little increase in SV

35. >120
Aortic valve pathology
+Pressure Gradient =
Aortic stenosis
-Pressure Gradient=
Aortic Insufficiency
>15
Mitral valve pathology
Diastole
(V Filling)
Systole
When? Diastole =
Mitral stenosis
Systole =
Mitral Insufficiency
S1
S2

36. 𝑇𝐿𝐶 = 𝑉𝐶 + 𝑅𝑉
𝑇𝐿𝐶 = 𝐹𝑅𝐶 + 𝐼𝐶
RATE DEPTH
Conducting
More CO2
Less O2
Low pH
Respiratory
Less CO2
More O2
High pH

37. DEAD SPACE
CONDUCTING
PO2 = 100
PCO2 = 40
PN2 = 600
PH2O = 47
RESPIRATORY
ZONE
PO2 = 100
PCO2 = 40
PN2 = 600
PH2O = 47
End of Expiration End of Inspiration
Same
composition
as respiratory
zone (CO2)
O2, N2, H20.
NO CO2 in
normal
atmosphere
Patm = 0Patm = 0
PA = +1 PA = 0
PA = -1 During mid-Inspiration
P = -4 P = -8
Recoil = +8Recoil = +5
RESTRICTIVE
diseases
OBSTRUCTIVE
diseases

38. Pressure is inverse to Volume
Ventilation:
Blood Flow:
Increased O2
Ventilation:
Blood Flow:
Increased CO2

39. 𝐶 =
∆𝑉
∆𝑃
A
B
Ageing
RD Syndrome
/ Atelectasis

40. RV
RV

42. Anemia
Polycythemia
Hemolysis
H+H+
Decreasing
affinity
Increasing
affinity

43. Alveolar
Ventilation
Chemoreceptors
Central
Medulla of the
brain
Main drive of VA
in normal
circumstances
Monitor
PaCO2
H+ ions
Peripheral
Around the
carotid sinus and
Aortic arch
Take over in
severe decrease
in PaO2
Monitor
PaO2
PaCO2 (less)
Excess in
Meningitis
Suppressed in
Opiates OD
Room air
21% of O2
<1% of CO2

44. PAO2 - PaO2 difference = 0-5 mmHg
Hypoxia
Hypoventilation
Decreased PaO2
A-a = 0
Decrease in
Alveolar vent.
TX= Oxygen
Diffusion
Impairment
Decreased PaO2
A-a = > 0
Lung Fibrosis
Give 100% O2
and redo.
Perfusion
Limited
Situation
Decreased PaO2
A-a = > 0
Pulmonary
Shunt
(Atelectasis)
Equilibrium capillary
– interstitium
Significant Increase (>10) = Diffusion Impairment
No Significant Increase (<10) = Pulmonary Shunt

45. If Glomerular Capillary Pressure goes
up = Increase in GFR,
if it goes down = decrease in GFR
PGC
PBS
πGC
πBS
8 mmHg
45 mmHg
0 mmHg24 mmHg
-
+
-
Freely filtered (1.0)
Electrolytes (Na+,Cl-,K+,HCO3)
Metabolic waste (urea)
Metabolites (glucose, aa)
Non-natural substances
(inulin, PAH)
Low-weight proteins (insulin)

47. If the substance has the same dynamics or
use the same transporter but nothing
changes while adding one or other, they
have to be transported by simple diffusion.
Facilitated
transport
FASTER
TM = Transport Maximum
Secondary active transport: Depends
indirectly on ATP as a source of energy.
Eg. Cotransport of Na-glucose in PCT
ATP is consumed directly by the protein
UREA is freely filtered,
flow dependent.

48. (mg/ml)
GFR= 120 ml/min
If you decrease GFR, you
decrease the filter load of
glucose and increases the
threshold.
In pregnancy GFR is
elevated, so T is lower.
Glucose will appear in
the urine at a lower
concentration.
𝐹𝐿 = 𝐺𝐹𝑅 × 𝑃𝐺𝐶
FL = Filter load
PGC = Plasma Glucose Concentration
𝐸 = 𝑈𝑥 × 𝑉
E = Excretion
Ux = Urine concentration of substance
V = Urine flow rate

49. 20%
120 ml/min
80%
480 ml/min
100%
600 ml/min
Protein Inulin = GFR Na, K, Urea
PAHGlucose,
Bicarbonate
Creatinine

50. 600
200
100
0
Inulin
PAH
Creatinine
Glucose
Volume filtered in
Bowman’s Capsule
80% delivered to
peritubular
capillaries
Plasma Concentration (mg/dl)
Zero clearance
at lower
concentrations
Carrier Saturation,
no longer 100%
filtered

51. 60% Retained
at the PCT
Osmotic
Gradient
Diluting segment –
Greatly decreases Osm
K+
Na+
H+
5a
5b
Aldosterone
Lithium
Clearance
Na+
K+
40 ml/min
Urea
PTH
Phosphate
Vitamin D
Ca++ Inhibits
K+ Inhibits

52. Fanconi Syndrome

53. Acidosis Alkalosis Compensation
pH Low High
Respiratory
PCO2
High Low Only Renal
Metabolic
HCO3
Low High Ac. Hyperventilation
Alk. Hypoventilation
Renal
If both present:
Mixed
pH: 7.4
HCO3: 24 mEq/L
PCO2: 40 mmHg
Renal Compensation:
Lowers plasma HCO3 by
excreting it
Raises HCO3 by generating
new
𝑁𝑎
+
= 𝐶𝑙
−
+𝐻𝐶𝑂3 −
Plasma Anion Gap
140 108 24
132

55. PCO2
Increase
PCO2
Decrease

56. 1. Fast – Short half-life
2. Non-protein bound
(except IGF)
3. Excreted in urine
4. Activates a protein
5. Have second
messengers
1. Slow – Long half-life
2. Protein bound (except
for DHEA)
3. Not excreted
4. Makes a protein
5. Pulsatile (except
Thyroid)
Regulated
Feedback Inhibition
Effect on an organ

57. Permissive Action
Growth HormoneThyroid
Glucagon, CatecholaminesCortisol
Fast, Arginine and
hypoglycemia stimulates it.
Elevated during sleep
Overnight
Dexamethasone
suppression test
Elevated in the morning
TRH Thyrotrophs (10%) TSH
CRH Corticotrophs (10-25%) ACTH
GnRH Gonadotrophs (10-15%) LH, FSH
GHRH Somatotrophs (50%) GH
SST
Dopamine Lactotrophs (10-15%) Prolactin
TRH (elevated)
+
+
+
+
+
-
-

58. Stress Hormones
1. Growth Hormone – Increases protein formation from A.A.
2. Glucagon – Takes aminoacids and uses for gluconeogenesis
3. Epinephrine – No effect on proteins
4. Cortisol – Promotes degradation on proteins
Anabolic Hormones
1. Thyroid hormone
2. Growth Hormone
3. Insulin
4. Sex Steroids (mainly Testosterone)
Raises:
Glucose
Free fatty acids
Lipolysis

59. Zona Glomerulosa
Zona Fasciculata
Zona Reticularis
Capsule
Medulla
ACTH
Cortisol and
Androgens
Aldosterone
80% Epinephrine
20% Norepinephrine
Angiotensin II, K+
ANS
REGION HORMONES CONTROLLED BY

60. Cholesterol
Pregnenolone
Mineralocorticoid
(11-deoxycorticosterone)
Cortisol Sex Steroids
Mineralocorticoid
(Aldosterone)
21-h 21-h11-h
11-h
21-hydroxylase deficiency
VS
11-hydroxylase deficiency
SALT-WASTING sx with
Hyperkalemia and Hypovolemia,
Hypertension
17-h
LDL Acetate
Glomerulosa
Fasciculata
Reticularis
Conn Syndrome –
Hypertension + Hypokalemia
Deficient in ALL of them.
Lack of feedback inhibition
leads to Increased ACTH

61. Plasma Osm Urine Osm Plasma ADH Urine Osm Post-
desmopressin
Normal 297 814 Elevated 815
Central Diabetes
Insipidus
342 102 Decreased 622
Nephrogenic 327 106 Elevated 118
1 mg overnight
dexamethasone
High dose
dexamethasone
ACTH level
Suppressed Normal Pituitary source Adrenal source
(feedback inh)
Not Suppressed Hypercortisolism Ectopic ACTH,
adrenal tumor
Pituitary or
Ectopic source

63. Insulin
• Protein Synthesis
• Glycogenesis
• Lipogenesis
• Glucose Oxidation (muscle)
• Increases glucose
• Increases fatty acids
• Increases IGF – make proteins
Glucagon
• Ureagenesis (protein
metabolism)
• Glycogenolysis
• Lipolysis
• Gluconeogenesis
• Ketogenesis (fatty acids
metabolism)
• Insulin secretion
Growth Hormone

64. Dihydrotestosterone in the baby:
Makes penis, prostate and
scrotum
Dihydrotestosterone in the adult:
Male pattern baldness and BPH
Testosterone in the baby:
Vas deferens, seminal vesicle,
epididymis.
Testosterone in the adult:
Maintains Sertoli cells - semen
Leydig
Sertoli /
Semen
Leydig
Both
Müllerian Inhibiting Factor:
Inhibits growth of female
internal structures.
Leydig makes Estradiol

65. Variable
14 Days
Yellow
LH-
-
Estrogen
+
-
β-HCG rescues
corpus luteum
during pregnancy

66. Hormone Source Stimulus Stomach Motility
and Secretion
Pancreas Gallbladder
Secretin S cells lining
duodenum
Acid entering duodenum,
activates CFTR via Gs
Inhibits Stimulates fluid secretion
(HCO3) and Bile into bile
canalicular ducts.
CCK Cells lining
duodenum
Fat, peptides and amino
acids entering duodenum
Inhibits emptying Stimulates enzyme
secretion (Amylase,
lipase, protease)
1. Contraction
2. Relaxation
of Oddi
Sphincter
Gastrin (ACh)
Feedback
inhibition with
acid or SST
G cells of the
stomach
Stomach distension
(stretch)
Stimulates
motility
Antrum Parasympathetic (GRP),
Peptides (protein)
Activates Pepsin,
acid production
Duodenum Stomach and acid inhibits
GIP (Gastric
inhibitory peptide)
GLP
Duodenum Fat, Carbohydrates, amino
acids
Inhibits High increase of insulin,
decreases glucagon
All four hormones stimulate Insulin release.
CCK, GIP and Secretin increase pyloric constriction, slow stomach emptying.

67. Duodenum – Fluid remains isotonic.
Absorption of ions and water-soluble vitamins
begin. Iron (ferritin) and Ca+ absorption
(calbinding and calcitriol).
Jejunum –Net reabsorption of ions and water-
soluble vitamins.
Ileum – Net reabsorption of water, Na+, Cl- and
K+. Secretion of HCO3
Distal Ileum – Reabsorption of bile salts and
Intrinsic factor with Vitamin B12
Colon – Doesn’t have digestive enzymes.
Net reabsorption of water and NaCl. Target for
Aldosterone, increases Na+ and water
reabsorption and K+ secretion.