Download Dear Notetaker:

BHS 116.2 – Physiology
Notetaker: Vivien Yip
Date: 2/6/2013, 1st hour
Page1
Final Exam Review
**Not inclusive, anything covered during the quarter may appear on the exam
65- 66 Questions
(New) GI/liver material will make up 2/3 of exam
Chemical structure of hormones
- Proteins, peptides
- Steroids
- Tyrosine derivatives
- Signaling and target cells
- Plasma receptors
- Signalling cascades lead to end result
- Cyclic amp cascade
- Gq phospholipase C cascade
- Steroid hormone and thyroid hormone
o Lipid soluble can directly diffuse to target cell
o Bind nuclear receptor
o Sometimes cytoplasmic receptor
o Hormone receptor complex that activates transcription
Anterior pituitary hormones
- Not tropic
- What they are
- What they do
- All of them are tropic except prolactin
- Stimulate targets to secrete another hormone
- Prolactin is the only one that does not do that
Hypothalamic hypophyseal portal system
- Anterior pituitary secretion relies on releasing factors/inhibiting factors released from hypothalamus
- Stimulate or inhibit anterior pituitary cell to secrete their hormones
Regulation of anterior pituitary hormone secretion
- Negative feedback from the end hormone back onto the anterior pituitary and or the hypothalamus to
inhibit secretion
- Final hormone will have its own target
- Once there is enough of target hormone in the blood, no need for anterior pituitary or hypothalamic
hormone to continue secretion
- Rarely will see anterior pituitary hormone
- Only the target that is involved in negative feedback process
Main stimuli: GH
- Stimulating and inhibiting factor released by hypothalamus
- Inhibitory: somatostatin
- Stimulatory: GHRH
- Depending on which factor is released, will get stimulation or inhibition of GH release
- GH has different effects on target
o Metabolic
 Triggered by GH itself
o Growth promoting actions
 Carried by IGF 1
 GH stimulate liver to secrete IGF1
 IGF trigger growth in target tissue
Posterior Pituitary
- 2 hormones released
BHS 116.2 – Physiology
Notetaker: Vivien Yip
-
-
Date: 2/6/2013, 1st hour
Page2
Produced in the hypothalamus
o ADH/vasopressin
o Oxytocin
No hypophyseal portal system
Axons of neurons that travel through pituitary stalk and release hormone in the posterior pituitary gland
Pathologies
- Pituitary adenoma (anterior pituitary)
o Visual system symptoms are due to compression of nerves
o Bitemporal hemianopsia (optic chiasm is compressed)
o Optic atrophy (compression of chiasm lasts a long time will stop blood supply)
o Lateral growth (into cavernous sinus) will compress cranial nerves that supply the EOMs 
diplopia
o Hormonal symptoms: whichever cell type is oversecreting
- Diabetes insipidus (posterior pituitary)
o Excess urination due to excess water in the body
o Hypothalamic or posterior pituitary damage
o Decreased or no ADH secretion
o Body is unable to reabsorb the water from renal tubules
Thyroid Hormone Synthesis
- Requires iodine
- T3 and T4 are the primary thyroid hormones
- T4 is most abundant
- T3 is most active and efficient at stimulating activity
TH Secretion
- Primary action on target is to increase metabolism
- Increase metabolic rate
- Permissive action: increases ability of other hormones to work (sympathetic nervous system)
o Increase/enhance sympathetics
Hyperthyroidism
- Thyrotoxicosis – excess thyroid hormone
o Negative feedback leads to very small amounts of TSH
o Elevated T3 and T4
Graves Disease
- Most common of hyperthyroidism
- Autoimmune disease
- Antibodies stimulate the TSH receptor
- TSH receptor is constantly stimulated
o TSI
o TBII
o TGI
Thyroid Adenoma
- NOT autoimmune disease
- Secretory function of the rest of the normal thyroid gland is shut down
- Decreased TSH
- Cancerous part of gland hypersecretes thyroid hormone
- Genetic analysis indicates mutation in TSH receptor (as if constantly active)
Hypothyroidism
- Hashimoto thyroiditis
- Decreased thyroid hormone secretion
BHS 116.2 – Physiology
Notetaker: Vivien Yip
-
Date: 2/6/2013, 1st hour
Page3
Autoimmune disease that destroys the gland itself
TSH levels are high
Lack of negative feedback
Goiters
- Endemic goiter pathology
o Due to iodine deficiency
o Elevated levels of TSH
o Unable to produce mature thyroid hormone
- Idiopathic nontoxic goiter pathology
o Normal iodine levels
o Mild thyroiditis
o Abnormal thyroid enzyme systems
Adrenal Cortex
- Mineralocorticoids
o Zona glomerulosa
o Aldosterone
o Major regulator in electrolyte and water balance
- Glucocorticoids
o Cortisol
o Zona fasiculata
o Role in CHO, fat and PRO metabolism
- Androgens
Aldosterone
- Increases renal K+ secretion
- Increase renal reabsorption of Na+
o Increase in H2O retention
- Net effect is to increase the total amount of Na+ and decrease K+ in the ECF and to increase ECF volume
o Important in long term maintenance of blood pressure
Cortisol
- Released in response to mental or physical stress
- Transmit signals to hypothalamus
o Release CRH
- Stimulates anterior pituitary
o Release ACTH
- Stimulates cortisol release from adrenal cortex
- Increase blood glucose
o At the expense of protein and fat stores
- Enough glucose for brain and skeletal muscles
o Triggers insulin resistance in other tissues
- Elevated amino acids and fats as well
Adrenal medulla
- Modified part of sympathetic nervous system
- Release catecholamines: epinephrine (adrenaline) and norepinephrine
o Both are tyrosine derivatives
Calcium Absorption
- Body keeps a tight regulation on the ECF concentration of Ca2+
- Slight changes can induce a large change in the body
- Calcium intake from diet will make its way out of the body at some point
- If not enough coming from diet, bone will be major source of calcium
BHS 116.2 – Physiology
Notetaker: Vivien Yip
Date: 2/6/2013, 1st hour
Page4
Vitamin D
- Formed in the skin
- Natural precursor with the help of sunlight
- Absorbed mostly through diet
- Required to absorb calcium from digestive system
o Need active Vit D3 to do this
- Add 1 hydroxyl group in the liver
o Requires PTH (major) or decreased phosphate levels in blood to trigger 2 nd hydroxyl reaction in
the kidney
o Now get active form of Vit D3
o That can now stimulate absorption of calcium and phosphate from GI tract
Parathyroid hormone (PTH)
- Acute and chronic effects
- Primary job is to raise plasma calcium levels
- Acute form
o Stimulate osteocytes and osteoblasts
o Remove calcium from the amorphous pool of calcium salts
o Short term elevation of PTH response
- Chronic
o PTH always present
o Osteoclasts are activated
o Break down mineralized bone
o Release both calcium and phosphate into the blood
Bone production and calcification
- Amorphous pool (first source for calcium)
- If chronic effects,
o Break down bone by activating osteoclasts
PTH effects on ECF concentration of Ca2+ and PO4- Trigger kidneys to excrete phosphate
- Decrease plasma levels of phosphate
- PTH also stimulates kidneys to reabsorb calcium
- Increase plasma concentration of calcium
Regulation of plasma Ca++ by Vitamin D & PTH
- Increase dietary uptake of calcium
- Increase renal tubule reabsorption of calcium
- Stimulate bone to mobilize calcium
- Act on bone and kidneys directly
- Indirect action on intestines through Vit D
Negative feedback with PTH and calcitonin secretion
- Elevated calcium levels trigger calcitonin
- Decrease calcium levels back to normal is the goal of calcitonin
Osteoporosis
- Occurs naturally w/ age
- Decreased mineralization
- Senile osteoporosis
o Reduced bone formation
o Reduced osteoblast activity
- Postmenopausal
o More severe
o Decreased osteoblast activity and bone formation
o Increased osteoclast activity and bone resorption
BHS 116.2 – Physiology
Notetaker: Vivien Yip
Date: 2/6/2013, 1st hour
Page5
Addison Disease
- Hypoadrenalism
o Affect aldosterone and cortisol levels
- Primary adrenal insffucieicny
o Autoimmune adrenalitis
o Infections
o Metastatic neoplasms
Cushing Syndrome
- Hypercortisolism
- 4 causes: pituitary cushing, adrenal cushing, paraneoplastic cushing, iatrogenic cushing (most common
cause)
Hypothyroidism
- Not very common
- Parathyroid gland does not secrete sufficient PTH
- Hypocalcemia
- Not triggering the kidneys to resorb more calcium
Primary hyperparathyroidism
- Hypercalcemia
- Hypersecretion of PTH
Secondary hyperparathyroidism
- Vit D deficiency
- Renal disease
o Cause hypocalcemia
o Constantly stimulating parathyroid gland
Pancreas
- Alpha cells
o Glucagon
- Beta cells
o Insulin
Insulin Receptor
- Once bound, becomes an active enzyme
- Triggers GLUT 4 to be inserted into membrane
- Makes target tissue permeable to glucose
- Most tissues are impermeable to tissues except brain and liver without insulin
Insulin target tissues
- Adipose
- Liver
Regulation of insulin secretion
- Blood glucose increase
- Insulin secretion increases
- Storage hormone, reduce glucose levels
- Promotes storage for long term use fo glucose fat and amino acids
Glucagon
- Responds to decreased blood glucose levels
- Triggers an increase in blood glucose
- Insulin and glucagon act oppositely
Type 1 diabetes
BHS 116.2 – Physiology
Notetaker: Vivien Yip
-
Date: 2/6/2013, 1st hour
Page6
Autoimmune
Hyperglycemia
Insulin deficiency
Attack on beta cells, preventing insulin release
All other symptoms stem from hyperglycemia
Type II diabetes
- Insulin resistance initially
- Later on, can result in insulin deficiency
- Know long term effects
- Sorbitol pathway
Alimentary Tract
- Functions: move food through, digestion, absorption of nutrients
- Regulatory mechanism: nervous and hormonal
- Cross section of gut
o Mucosa
o Submucosa
o Muscularis externa
 Outer longitudinal layer: peristalsis
 Circular layer: mixing
o Serosa
Slow wave potential
- Smooth muscle
- Interstitial cells of Cajal
- Slow wave of subthreshold depolarization
- If triggered by depolarizing factors near threshold
- Stretch, Acetylcholine, parasympathetics and GI hormones
- Know the difference between depolarizing and hyperpolarizing factor
Enteric Nervous System
- Myenteric
o Control movement
o Peristalsis and mixing
- Submucosal plexus
o Control secretion of GI tract
Ingestion of Food
- 3 stages
o Voluntary
o Pharyngeal
o Esophageal
Function of Stomach
- Storage of food (main function)
- Start digestive process
- Antrum: thicker muscular layer and pushes food through pyloric sphincter to duodenum
- Pyloric pump
o Strong contractions and push a little bit of chime each time
o It is always released in very small amounts to digest in small intestines
Regulation of stomach emptying
- Amount of chyme stimulates emptying and motility
- Fluidity of chyme
- Enterogastric reflex
BHS 116.2 – Physiology
Notetaker: Vivien Yip
-
Date: 2/6/2013, 1st hour
Page7
Intestinal hormones (CCK, and secretin)
Released when food is pushed into small intestines
Movement of small intestine
- Gastroenteric reflex
o Initiated by distension of stomach
o Increases motility
- Hormonal control
o Gastrin, CCK, insulin and serotonin all increase intestinal motility
o Secretin and glucagon inhibit small intestine motility
Movements of Colon
- Main storage
Secretion of Saliva
- Salivary amylase, begins CHO digestion
- Breakdown complex starches into simpler sugars
- Lysozyme, breakdown bacterial cell walls
- Antibody IgA also attacks bacteria
- Mucus produced to help lubricate bolus of food to go down esophagus easier
- Ductal cells: absorb sodium and chloride
- Saliva is very devoid of sodium and chloride (we are very sensitive to salt)
Summary of Gastric Secretion
- Know what each of these cells secrete and what is triggering their secretion:
- Mucous cells: protective mechanism
- Chief cells
- Parietal cells
- Enterochromaffin cells
- G cells
- D cells
- Acetylcholine produced by nervous system will stimulate the activity of most of these cells
- Major inhibitory factor will be the somatostatin produced by D cells
- Pepsinogen is an inactive enzyme
o HCl is used to convert into the active pepsin
o Pepsin can convert more pepsinogen to active pepsin
Phases of Gastric Secretion
- Cephalic phase
o Sight and thought of food
- Gastric Phase
o Most abundant secretions occur when food has entered the GI
o Once food leaves, there is a decrease in gastric secretion
- Intestinal Phase
Pancreatic Secretion
- Exocrine portion: key role
- Glandular cells will secrete digestive enzymes
- Ductal cells secrete sodium bicarbonate to decrease acidity of chyme
- Protect smooth muscle epithelium
- Major enzymes involved are produced by pancreas
- Only enzymes before that is salivary amylase and pepsinogen in the stomach
- Primary enzymes produced by pancreas
- Proteases will be inactive (activated in small intestine)
- Trypsinogen to trypsin
- Pancreatic amylase is released in active form
BHS 116.2 – Physiology
Notetaker: Vivien Yip
Date: 2/6/2013, 1st hour
Page8
Regulation of Pancreatic Secretion
- Food in the duodenum primarily fat and protein trigger CCK release
- CCK stimulate glandular/acinar cells to release pancreatic ezyme
- Acetylcholine can also stimulate glandular cells
Secretion of Bile by liver
- Stored in gall bladder
- CCK triggers release
- Emulsify fats so that pancreatic lipase can break down more easily
- Role in transporting products
Digestion and Absorption of Carbohydrate Summary
- Know the breakdown to absorption
- Begins digestion in the mouth
- Continues in small intestine
- Epithelium of the small intestine (enterocytes) have small enzymes attached to its surface
- Final digestion of carbohydrate and protein occurs in the enterocytes
Glucose and galactose are taken up via co transport
- Fructose is taken up by itself via facilitated diffusion
- All 3 are transported out into the blood
Protein Digestion
- Starts in the stomach
- Pepsin is the first enzyme
- Mostly digested by pancreatic proteases
- Aminopeptidase on surface of enterocytes are taken up
- Amino acids are taken up via co-transport with sodium
- small peptides taken up via hydrogen co-transporter
- Only small amino acids are released in the blood
Fat digestion
- mechanical breakdown occurs via mixing movements
- bile breaks down larger fat particles into smaller manageable particles
- Triglycerides become free fatty acids and monoglycerides  still lipid soluble
o bile salts brings these to surface of enterocytes
o can diffuse directly into target cell
- Repackaged into triglycerides
o form chylomicrons, large lipid particles
o chylomicrons are exocytosed out of the enterocytes
o enter lymphatic system
o bypass portal system
o eventually makes it to circulation to liver where it is processed