p 5 py

Nephron blood flow

afferent arterioles, glomerulus, efferent arterioles, peritubular capillaries back to the veins

Filtration

glomerulus into the Bowman’s capsule

Reabsorption

lumen to peritubular capillaries (gets back to blood)

Secretion

peritubular capillaries to the lumen (ends up in the urine)

Potassium

does secretion

Freely filtered

substance in bowman's capsule has same concentration as in afferent arterioles. Proteins not filtered

Micturition

1. Contraction of bladder smooth muscle by parasympathetic 2. Relaxation of internal sphincter 3. Relaxation of external sphincter = voluntary

Micturition

bladder fills progressively until the stretch in its walls rises above a threshold level then a nervous reflex (micturition) reflex occurs that empties the bladder

Response to stretch BP

GFR is regulated by myogenic

BP is up

afferents contact

BP is down

afferents relax

Juxtaglomerular autoregulation

response to sodium flow past macula densa cells (if flow high to low send a paracrine signal to afferent to contract) (if signal is low signal to relax)

Loop of henle countercurrent multiplier

sets up the osmotic gradient in the medulla

Counter exchanger

vasa recta maintains the gradient

Descending loop only has water channels (no sodium channels)

why osmolarity increases down the descending loop

Ascending loop

Na pumped out at the

Descending loop

water moves osmotically

Descending loop

no sodium movement

Ascending loop

no water movement

Loop of henle does not work

ADH would not function and you would not get water reabsorption in the collecting duct

Proximal tubule

under normal conditions blood glucose under 180 is reabsorbed in the

180

reabsorption is linearly related to levels until

Blood levels exceed 180

glucose appears in the urine when

ADH accounts for

water reabsorption in the collecting duct

Increases in renin or osmolarity

ADH released in response to

Renin

response in low blood pressure/sodium flow

Decrease osmolarity

want to increase water to

What stimulates aldosterone release

increase in renin, increase in blood K (not dependent on renin, direct effect), decrease in BP (renin release)

Low BP

renin increases angiotensin I and angiotensin II directly

Liver

Angiotensin II is produced in

blood vessels stimulating vasocontraction

Angiotensin II acts directly on

Aldosterone causes

sodium reuptake in the cortex (increase in blood pressure)

Renin increases when

BP decreases, low blood volume, decrease in blood sodium low sodium past macula densa cells, sympathetics

What would happen with a decrease in blood volume

BP decrease would increase renin release and result in vasoconstriction of arterioles and decrease in GFR. also increase sympathetics which decrease GFR.

What happens when you increase ANP

1. decrease renin release, angiotensin II, aldosterone, ADH, inhibits Na and water reabsorption. Increased urine volume

Decrease 2. Decreased sympathetic activity = decreases vasoconstriction 3. Increases GFR

PTH

increases calcium reabsorption 1. Increases # of transporters on the apical membrane resulting in increase in transcellular transport 2. There is paracellular transport but is not increased

What does the kidney do if pH decreases

proximal tubules 1. Reabsorb bicarbonate that has been filtered 2. Make new bicarbonate (when you make new proximal tubules you also get NH3 and excrete it)

How does the kidney handle nonvolatile acids

takes CO2+ O2 and makes carbonic acid, comes out as H+ + bicarbonate excrete H+ and it absorbs bicarbonate

production of HCO3 in alpha intercalated cells and then absorbed

excrete H+

correct acid

Alpha intervalated

correct base

Beta intervalated

Excrete H+

production of HCO3 in alpha cells absorbed

Cephalic phase

just seeing, smelling, and tasting food

Migrating motor pattern

peristalsis sweeping between meals (fasting) sweeps undigested food through SI to LI

Pharyngeal phase

under autonomic control, SM (swallowing center of brain stem)

Mucosa layer

absorptive layer of GI, submycosal fibrous contains blood vessels and lymphatic vessels

Cephalic phase

vagus N (para) and hormones

Histamine

endocrine into blood, stimulation parietal cells to excrete HCL

Chief cells

pepsinogen (gastric lipase)

Vagus nerve

stimulate stomach motility

Gastric phase

food in stomach

Amino acid

use G cells to produce gastrin

Gastrin

released into the blood (hormone)

Gastrin stimulates

1. Histamine from ELC, 2. Pepsin from chief, 3. Increases motility of stomach, 4. pH 1 or below gastrin release inhibited, also direct effect of pH HCL release stopped

Intestinal phase

chyme reaches SI

Intestinal phase (when food enters SI)

1. CCK released 2. Secretin released 3. Moilitin released 4. Glucagon like peptide 1 released (bc increase glucose in diet)

Gastrin increases

SI and stomach motility

CCK stimulates

SI motility, slows gastric motility and secretions from pancreas and contraction of gallbladder

Pancreas

Secretin stimulates HCO3 from

HCO3 made in

mucous cells in stomach (low pH), brunner cells in SI, pancreas duct cells

Why HCO3 made

secrete mucous and HCO3 to protect epithelial cells and brunner/pancreas neutralize chyme that enters SI

Liver synthesizes

angiotensinogen synthesis, clotting factors/prothrombin/fibrinogen, converting bilirubin to urobilinogen in liver (occurs by bacteria in SI and LI)

Large intestine

absorbs water (less than SI)

Large intestine

no digestive functions, electrolytes (K, Na, Ca, Cl) vitamin B & K, aldosterone stimulates Na reabsorption (same mechanism as kidney)

Peristalsis

food moved by ____ in stomach

Segmentation

chyme sloshes between segments of SI that form when bands of circular muscles briefly contract

Stomach, SI

Peristalsis in the ____, segmentation in the ______

Parasympathetic nerves decrease

frequency and strength of contraction in SI (duodenum to ileum)

NO

causes relaxation of SM in SI

Carbs broken down

salivary amylase in mouth, pancreatic amylase in SI from asinar cells

Proteins broken down

stomach (pepsin acid), SI (many different enzymes)

Fats broken down

some in stomach (gastric lipase), mist in SI (pancreatic lipase)

Pancreatic lipase

bile made in liver and stored in gallbladder helps breakdown large lipid drops to small

Triglycerides (fats) broken into

monoglycerides/fatty acids by pancreatic lipase

Maltose/maltase

glucose/glucose

sucrose/sucrase

glucose/fructose

lactose/lactase

glucose/galactose

Zymogens

need to be processed (ex. Trypsinogen to trypsin)

Enterokinase

on epotheral cells, do not need to be converted (processed) from inactive to active

Fats

1. taken up by epithelial cells by passive diffusion 2. Remade into triglycerides and combined w/ protein to make chylomicrons 3. Chylomicrons taken up by lacteals of lymphatic system 4. Chylomicrons acted on by SKL M lipoprotein lipase to give fatty acids

Chylomicrons

too big for fenestrations , get back to blood

Skeletal muscles

use fatty acid as an energy source

Indefinite gonadas

begin with this, cannot tell gender

Testis Determining Factor (TDF) Y chromosome has SDY region that releases

TDF

causes testosterone

Male

from testes mullerian inhibitory substance causes degradation of mullerian duct

Female

lack of testosterone causes degradation of wolffian ducts

Male

mullerian ducts

Female

wolffian ducts

Epididymis, vas deferens, seminal vesicles, penis

Testosterone causes wolffian ducts to develop into male reproductive structures

Pubertal events in male and females

Increasing GnRH (pulsating) stimulates

Seminal vesicles

fructose, alkaline solution

Prostate

Ca, citric acid, coagulation proteins, fibrinolysin

Bulbourethral glands

mucus to lubricate urethra

False puberty (adrenarche)

8/14 yrs, growth of pubic and axillary hair due to androgen secretion from adrenal cortex

Leydig cell

Male cell produce testosterone

Thecal cell

female cell produce testosterone

Epididymis

Sperm gain requirements to be mobile in

Female reproductive tract

Sperm become fully mobile in