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255 Cards in this Set

  • Front
  • Back
acute renal failure defnition
decline in renal function within 24-48 hours
acute renal failure symptoms
reduced GFR
decreased urine output
azotemia (uremia)
Azotemia (Uremia)?
nitrogen waste products in blood (creatinine)
during acute renal failure
elevated BUN
acute renal failure causes
not enough blood flow to kidneys
either low blood volume
or constricted afferent/dialated effarent glomerial arteriols
glomeriolar inflamation
systemic lupus erethymatosis
epithelial cells break off clog nephron
plugs in later than nephron
common causes of chronic renal failure
diabetes
hypertension
glomerulonephritis
polycystic kidney disease
is chronic renal disease reversable
no
what is the declining cycle of renal disease
Primary kidney disease
decreased number of nephrons
hypertrophy and vasodilation of surviving nephrons and at the same time an increase in arterial pressure due to the decrease in the number of functioning nephrons
increased glomerular pressure and filtration in remaining nephrons
glomerular sclerosis
decreased number of nephrons
and the cycle continues
what are the two compensetory mechanisms in renal disease that lead to increased GFR
more prosteglandins: afferent vasodialation
angiotensin II: efferent vasoconstriction
stage 1 numbers
> 90ml/min
stage 2 numbers
60-90ml/min
endocrine glands are what tissue
epithelial
endocrine glands secret into what
blood stream
what are neuroendocrine cells
neurons that secret stuff into blood stream
the release of peptides are similar to what type of release in neurons
ca mediated exocytosis
how many ca domains are their in neuroendocrine cells
one
do neuroendocrine cells constantly need activation to release peptides by ca
no, some peptides are perminatly activated by ca
do hormones affect take place at the same pace
no, growth hormones for example are slow, adrenaline for example is fast
do hormone receptors have high or low affinity for hormones
very high
which type of hormones are bound to plasma proteins
steroids and thyroid hormones
what is the metabolic clearance rate
rate of clearnace of hormone/concentration of hormones in plasma
how are hormones cleared
metabolism
tissue binding
excretion of bile
urine
leptin
adipose tissue
appetite, metabolism, reproduction
cortisol
adrenal cortex
metabolism
stress
immune system
devolopment
androgens
adrenal cortex
sex drive in women
menstration
aldosterone
adrenal cortex
na/k secretion in kidneys
epinephrine
norepinephrine
adrenal medula
metabolism
cardiovascular function
GI tract hormones and what they do
gastrin (GI motility and secretions, pancreus secretions)
secretin (bile from galblatter)
cholecystokinen CCK
glucose-dependent insulinotropic peptide (GIP)
motilin
estrigen
progesterone
overies
reproductive system
breasts
growth and development
development of ovarian follicules
inhibin
secreted by ovaries
FSH secretion
relaxin
secreted by ovaries
helps relax birth canal
where is the pituitary gland
in a bony hole in the midbrain called the sella turica
pituitary gland is superior to what, and what connects it
hypothalamus
pituitary stock (infundibulum) (blood vessels and axonal projections)
pituitary gland is divided into which two parts
anterior
posterior
which part of the pituitary gland is an outgrowth of the brain
posterior
which hormones to the anterior pituitary secrete
what do they do
Growth hormone
adrenocorticotropic hormone (affects secretion of adrenocortico hormones)
thyroid stimulating hormone
prolactin (mamory gland developement, milk production)
FSH and LH (control steriod secretion of the overaries and testes)
What cell type makes up anterior pituitary
multiple cell types
what does the posterior pituitary secrete
what do these hormones do
ADH (anti diuretic)
oxytocin (milk letdown, baby delivery, orgasm)
what is the interface between neuron and endocrine system
hypothalumus
how does the hypothalumus control the secretions of the pituitary gland
secretions through the blood portal system (hypothalamic-hypophysial portal vessels)
what is positive and negative feedback for GH
GHRH and SS
positive and negative feedback for prolactin
no positve
dopamine negative
hypothalmic and pituitary hormones are all what kind of hormones
peptides (except dopamine, which is negative feedback for prolactin)
how do hypothalmic releasing factor's activate pituitary hormones
heterotrimeric GPR's, than PLC (IP3 and DAG), or AC (cAMP)
which pituitary hormones create their affect directly with no intermediate affects
prolactin and GH
what does GH affect
increase metabolism
increase protein synthesis
increase insulins effect
increase fatty acid use and gluconeogenesis
over all increase of blood glucose (like diabetes II)
what does GH need to exert its effects
it needs adequate carbohydrates
how does GH mostly affect bone growth
stimulates osteoblasts
GH can also act through which intermediat
insulin-like growth factor in the liver
which is the most important insulin-like growth factor
somatostatin C
what can cause GH to increase
starvation or protein defeciency
tertiary hypothyroidism
hypothalamic dysfunction
signs and symptoms of hypothyroidism
weight gain
cold intolerance
thin brittle hair or fingernailes
congnitive dysfunction
dyspnea on exertion
goiter
chain to secretion of thyroid hormone
anterior pituitary (TSH)
Thyroid (AC, cAMP, protein kinase A, protein phophorylation, thyroid hormones)
Thyroid hormone negative feedback on what
anterior pituitary, Hypothalmas
drugs that induce hypothyroidism
amiodarone
propylthouracil (block peroxidase enzyme)
methimazole (block peroxidase enzyme)
lithium
testing for hypothyroidism
TSH (how much tsh is in blood)
T4 levels
ultrasound neck area
biopsy
symptoms for autoimmune hashimoto throiditis
T4 decreased
TSH elevated
T3 resin uptake decreased
throid antibodies increased
treatment for hypothyroidism
levothyroxine (synthetic T4)
take for rest of life
surgery for goiter
graves disease
autoimmune disorder for hypoerthyroidism
graves disease mainly effects males or females
females
when are most patients diagnosed with graves disease
20-40
risk factors for graves disease
genetic
high iodine intake
stress
sex steroids
smoking
signs and syptoms of hyperthyroidism
fatigue
sweating
difficulty sleeping
nervousness
cardiovascular events
irregular menstrual cycles
sensitivity to heat
tremors
exophthalmos (protusion of eyeballs)
goiter
infiltrative dermopathy (thickening of skin near tibia and ankles)
pathophysiology of graves disease
HLA-DR gene (MHC antigen presentation)
CTLA-4 (t-cell inhibition)
mutant antibody (TSHR antibody)
90% of patients have this increase
TSRH acts as a substrate for TSH receptor
where is the thyroid gland
below the larnyx
on both sides of the trachea
how much can the thyroid glands change metabolism
50% increase or decrease
what is the hormone pathway to secrete T3 and T4
hypothalmus (TRH) (
anterior pituitary (TSH)
thyroid gland
what does TRH do in the anterior pituitary to release TSH
g protein
phospholipase
IP3 DAG
Ca influx
signaling pathway of TSH on the thyroid
acts on follicular cells
G protein
AC
increase cAMP
proteolysis of thyroglobulin
increase iodide pump
iodination of thyroglobulin
increase # and size of follicular cells
what is the thyroid gland composed
cuboidal ephithelial cells in round follicals which has T4 and T3 attatched to thyroglobulin molicules and C cells which secret calcitonin
what is the difference between the structure of t4 and t3
the iodine substituents on the iodine molecule
what is the primary t secreted by the thyroid gland
what is the primary t hitting receptor molecules
t4
t3
which t is most potent
t3 is 4x more potent than t4
which t has the shortest half life
t3
how does I get absorbed by the body
taken out of the blood by thyroid follicular cells TSH
How does I end up as t4
I (peroxidase to)
I3- --> iodinase to
Monoiodotyrosineor Diiodotyrosine --> 2 DIT's are T4, DIT + MIT --> T3
how are T3 and T4 released
follicular cells pinch off a vesicle with thyrobullin inside a cell
fuses with a lysosome
proteases digest thyrobullin releasing T4 and T3
some iodinated tyrosin residues are not released but are broken down and recycled deiodinase
how much T3 and T4 can the thyroid store
2-3 months worth as colloids of thyroglobullin
99% of T3 and T4 are bound to what
thyroxin binding globulin
why is T3 and T4 bound
for slow release
T3 and T4's time to action
T4 2-3 days latancy 10-12 days max effect
T3 6-12 hours latency 2-3 days maximum
where do T3 and T4 act in target tissues
intracellularly to receptor + retinoid x receptor in nucleus
affects transcription of metabolism genes
receptors have a greater affinity for T3 or T4
T3
what intracellular effects to T3 and T4 do the most
increase number and size of mitochondria
increase activity of Na/K ATPase
what are some neccesary actions of T3 and T4 concerning childrens growth
general childrens growth stuff
brain developement
T3 and T4 general effects on body
increase all type of carbohydrate metabolism (gluconeogenesis, glycolysis, etc)
increase fat break down
decrease cholesterol, phospholipids, and triglycerides
increase vitamin requirements
more heart work
increase GI motility
inactivates glucocorticoids (causes more CRH, ACTH, and increase glucocorticoid synthesis)
thiocyanate (SCN-) effects
competes for I pump
Decrease iodinations of thyroglobullin
feedback increases TRH and TSH
hypertrophy in thyroid gland (goiter)
propylthiouricil (6propyl-2sulfonyl-pyrimidine-4-one) effects
blocks action of peroxidase
blocks coupling of MIT and DIT
positive feedback TRH and TSH
hypertrophy in thyroid gladn (goiter)
high levels of iodide effects
inhibit thyroid gland
decrease size (hypotrophy)
PTH regulates what
calcium and phosphate in the GI, renal secretion, and bone exchange
where is the PT
4 PT's are in posterior side of thyroid gland
types of cells in the parathyroid
chief cells secrete PTH
oxyphills (no important function)
PTH is synthesized as what type of hormone
prepro
kidneys does what to PTH
secretes it rapidly, but does not secrete its fragments which cause its effects
kidney stones male to female ratio
4 to 1
percentage of males likely to get kidney stones
10-12%
percentage of kidney stone reaccurance in affected people
50%
peak age of those with kidney stones
20-50 years old
what kind of kidney stones are with men
calcium oxalate
urate and cystine (with both)
what kind of kidney stones are with women
struvite
urate and cystine (with both men and women)
what causes symptoms from kidney stone
if above the pelvis no symptoms
problems when it is in the ureter and prevents dranage
stones in the proximal ureter cause what symptoms
pain in the anterior upper abdomen
stones in the distal ureter causes what symptoms
ipsilateral testicle
labia
stones in between ureter and bladder causes what symptoms
dysuria
urgency and frequency
may be mistaken for UTI
symptoms common to all location of kidney stones
blood in urine
nausea
vomiting
causes of kidney stones
supersaturations of minerals
calcium oxelate 70%
calcium phosphate 5-10%
Uric acid 10-15%
struvite 10-15%
cystine 1%
hypercalciuria
hyperuricosuria
hyperparathyroidism
what does low PH urine causes
uric acid stones
what does the proteus bacterial infections sometimes causes
sturuvite infection
pathophysiology of kidneys
postrenal acute renal failure (stops urine flow)
Decrease GFR
hyperkalemia
hypertension
edema (decrease in capillary oncotic pressure)
acidosis
azotemia (increase uria, creatinine, uric acid, BUN)
treatment and prevention of kidney stones
< 5 mm pass it, control pain, alpha 1 blocker relaxes ureter
> 5mm extracorperal shock wave lithotripsy, uretoscopy, percutaneous nephrolithotropy
life style changes when you have a kidney stone
increase fluids (water is best)
eat less calcium, vit D, etc.
Drug therapy for calcium stones
thiazide diuretics
uric acid stones drug therapy
alkali supplements
allopurinal
struvite stones drug therapy
antibiotics
most common human bacterial infection
UTI
long term catheter will cause what infection
UTI
what are risk factors for male UTI's
old
lower uti symptoms
dysuria
painful urination
frequent urges to urinate
suprapubic heaviness
nocturia
upper uti symptoms
flank pain
fever
nasea
malaise
asystematic UTI's occur in what people group
old people
what is a complicated UTI
one with a
lesion, stone, or other block
male infections
indwelling catheter
prostatic hypertrophy
upper UTI located where
kidneys
what are most uncomplicated UTI's caused by
E coli
what is the size difference between men and womens urethra
20cm vs 4cm
what helps prevent UTI's naturally
urine flow
urethral spincter (between bladder and ureter)
urine acidity
what is the definition of a complicated UTI
UTI's that are caused by other things
how to diagnose a UTI
urin culture (determine type of culture)
Urinalysis (wbc's, rbc's, nitrates, pyuria) (elevated wbc's means infection)
treatment for mild UTI's
antibiotics (usually bactrim, quinolones)
treatment for sever UTI
IV antibiotic
OTC treatment for UTI's
Azo's (will turn urine orange)
Uristate
inner adrenal medulla secretes what
catecholamines (principly dopamine)
Adrenal cortex secretes what primarily
Corticosteroids
mineralcoticiods (ie, aldosterone, mess around with Na, K)
glucocorticoids (ie, cortisol, mess with glucose)
where are the 2 adrenal glands
on top of the kidneys
what part of the adrenal cortex secretes aldosterone
zona glomerulosa
what part of the adrenal cortex secretes androgens and cotisol
zona faciculata (middle)
zona reticularis (inner, secretes Dehydroepiandrosterone (DHEA) and androstenedione)
what causes the secretion of cortisol, androgens and some estrogens
CRH in the hypothalimus
ACTH in the anterior pituitar
where in the cell are corticosteroids synthesized
mitochondria
ER
is cortisol a mineralcorticoid or glucocorticoid
glucocorticoid
is cortisol bound to plasma proteins or free
90-95% bound to cortisol binding globullin
half life is 60-90% since almost all of it is bound
is aldosterone bound to plasma proteins or free
60-65%
half life is 20-25 minutes because only partially bound
how is cortisol metabolized/secreted
metabolized in the liver in conjunction to glucoronic acid
changed to hydrophilic molecule that is 75% excreted in kidney
25% is secreted in feces
where does cortisol act in the target cell
intracellularly to affect DNA synthesis
what is the prepro hormone to ACTH/what does it do
Proopiomelanocortin (POMC)
also helps trigger MSH, b-lipotropin, b-endorphen
Prohormone Convertase is secreted by the pituitary and is in the process
alpha-, beta- and gama -MSH secreted how in the hypothalamus
hypothalamus has PC2 gene which processes Proopiomelanocortin (POMC)
MSH is important in regulating what?
skin pigmentation
cortisol imbalance will primarily effect what
metabolism and ability to deal with stress
95% of glucocortiod secretion is what
cortisol
cortisol also called
hydrocortisone
cortisol effects gluconeogenesis
release of enzymes
release of amino acids for gluconeogenesis
how does cortisol increase blood glucose
increase gluconeogenesis
decrease glucose utilization
decrease sensitivity to insulin
what is adrenal diabetes
cortisol causes an increase of 50% more glucose
where does cortisol cause an increase in proteins
liver only
how does cortisol affect adipose tissue
lipolysis through secretion of FA's
excess can cause fat deposition in stomach and head
cortisol in stress and inflammation
stress stimulates cortisol (mental and physical stress)
increase glucose and AA's for the resonse
saves vital proteins
stops inflammation)
How does cortisol decrease inflammation
stabilizes lysosomal enzymes
decrease proteolysis
decrease capillary permiability
decrease WBC chemotaxis
decrease phagocytosis
decrease production of leukotriensa and prostiglandins
suppress t-lympocytes
decrease release of interleukin-1 (usually stimulates fever)
reduce allergin reagin binding
decreases circulating eosinophils
decreases number of lymphocytes
atrophy of lymphoid tissue
increases RBC (polycythemia)
adrenal secretion of androgens
Dehydroepiandrosterone is the prepro hormone for male sex hormones
some estrigen and progesterone secreted as well
anatomy of pancreas
two types of tissue acini (exocrine), and isle of langerhan (endocrine), both epithelial
islets of langerhan are divided into alpha, beta, and gama
beta - insulin 60%
alpha - glucogon 25%
delta - somatostatin 5%
Insulin Structure, Metabolism, Transport and Mechanism of Action
2 peptide chains connected with 2 disulfide bonds
synthesized in rought ER to preprohormone
unbound with short half life
released by blood glucose levels (not hypothalamus/pituitary)
acts via RTK and phosphorylates

cleaved to proinsulin in ER
Insulin secretions
b-cells in pancreas have glucose transpoters that monitor how much glucose is in the blood
glucose is oxidized and turns into ATP
depolarizes b-cells by inhibiting K
once voltage gated Ca is activated, then exocytosis of insulin is activated
glucogon, GIP, and acetylcholin can increase Ca influx in the presence of insulin
somatostatin and NE inhibit insulin release
AA's cystine and arginine can help insulin secretion in the presence of glucose
insulin has a quick release, but as stores of insulin in b-cells are depleted, there is a slow release due to new insulin being made
hormones GI: gastrin, secretin, cholecystikinen (CCK), GIP
others: GH, cortisol, glucogon, progesterine, and estrigen can increase insulin secretion
How do sulfonylureas act
block K channels in b-cells
effects of insulin on blood glucose
skeletal, adipose, and liver are affected most by insulin
inbetween meals, muscles take up FA for fuel (almost no glucose)
during excercise muscle can act insulin independently
glycogen broken down between meals maintains glucose
insulin deactivates phosphorylase which breaks down glycogen
insulin activates glucokinase which stores glycogen
decrease insulin causes glucose phosphorylase to dephosphorylate glucose and maintain glucose levels
60% of glucose is stored as glycogen (if exceeded during on meal, excess glucose is stored as FA, transported as VLD lipoproteins)
blood glucose reaching less than 50% is dangerous in the brain
effects of insulin on fats
chronic increaase in insulin causes atherosclerosis
glucose-->pyruvate-->acetyl-CoA-->FA's
before ariving to adipose cells VLD must be broken down again to FA's by lipoprotein lipase
insulin inhibits hormone sensitive lipase
decreased insulin can stimulate hormone lipase
decrease insulin breaks down FA and causes increase acetoacetic acid (ketoacidosis) (excess FA's cause an increase in carnitine transport system, which increase beta-oxidation of faty acids in the mitochondria)
excess FA's synthesize phospholipids and cholesteral in the liver) (also less insulin means less utilization of acetoacetic acid)
effects on insulin on protein and growth
protein storage
uptake of AA's by cells
increase translation (ribosomes are inactive without insulin)
long term insulin increase protein DNA sequences
inhibits protein catabolism (opposes gluconeogenesis)
insulin and GH act together for protein anabolism
carbohydrate vs. fat metabolism by insulin, GH, cortisol, and adrenoline
insulin favors carbohydrate use (disfavors fat use)
GH and cortisol are stimulated by hypoglycemia, increase fat metabolism
adrenoline increases blood glucose by glycogenolysis and lipolypase
glucogon
released by alpha cells in pancreas
90mg% glucogon secretion can increase blood glucose 3 to 4 times
after high protein meals glucogoon is secreted for gluconeogenesis
excercise causese 4 to 5 times increase in glucogon secretion
stimulates glycogenolysis (g protein-->AC-->cAMP-->phosphorylase b kinase-->phosphylase b changed to a -->break down of glucose
increase gluconeogenesis in liver by converting pyruvate into phosphoenol-pyruvate
at high doses glucogon can:
increase heart strength
increase blood flow to kidneys
increase bile secretion (increase FA absorption)
decrease gastric acid secretion
somatostatin
secreted by delta cells in pancrease
stimulated by eating
increase blood glucose
increase AA
increase FA
increase GI hormone release
decrease secretion of insulin and glucogon
decrease GI motility
decrease GI absorption and exocrine secretions
over all slows down digestion and use of nutrients
diagnosis of diabetes
blood glucose levels
oral blood glucose test (ingest glucose and see how high and for how long glucose is increased)
c-peptide is released along with insulin, so you can measure that (usually low levels is diabetes)
measure ketone bodies
30% of americans are undiagnosed with diabetes
measure antibodies against GAD, Islet cells, and insulin
type 1 diabetes
genetic predisposition
autoimmune disease
may be triggered by viral infection
has been linked to DNA causes the release of MHC II protein
incidence has increased since WWII
high glucose causes
fast heart rate (actually increase in FA)
glucose in urine
dehydration
peripheral ischemia
nerve damage
ketone acidosis (compesitory is breathing out lots of CO2 and synthesize HCO3-)
protein catabolism
Type II diabetes
part of metabolic syndrome (obesisty, fasting hyperglycemia, lipid abnormalities, hypertension)
monogenic are 1-5% of diabetes in the younge (messed up glucokinase and beta cell monitoring of glucose)
may be due to free FA's and adipose tissue
decrease skeletal muscle insulin sensitivity by stoping IRS signalling pathway -->RTK-->MAPK and PIK
dysregulation of cytokine secretion in adipocytes
local inflamation-->TNF released from adipose cells-->block PPARy effects -->decrease insulin resistance -->poliferate b cells especially with high fat diets
autocrine/paracrine amylin may be involved
other causes:
cushing syndrome (increase in cotisol or steroid therapy)
acromegaly (increase in GH)
pregnancy (gustational diabetes)
polycystic ovarian disease
lipodystrafy (accumulation of lipids in the liver)
autoimmune destruction of insulin receptors
genetic obesity (melanocortin receptor mutations)
hemochromatosis (iron accumulation in tissues)
after insulin hypersecretion for a while type I diabetes develops after a while
Insulinoma- Hyperinsulinism
malegnant tumors in islet cells
hypersecretion of insulin
low glucose causes nervousness, some hallucinations, then seizure, loss of consciousness, then coma
treat with glucose/and or glucogon
etiology of hyperparathyroidism
risk increases with age
chief cell adenoma
hyperplasia (tumours in the pituitary and pancreas, pheochromocytoma (adrenal gland tumour), medullary carcinoma of the thyroid and hyperparathyroidism)
Secondary:
resistance to PTH-->hypocalcemia-->parathyroid hyperplasia
severe calcium and vit D defeciencies
chronic renal failure
osteomalacia

carcinoma
signs and symptoms of hyperparathyroidism
Bones, stones, abdominal groans and psychic moans
Skeletal: cortical bone loss, bone and joint pain, pseudogout, chondrocalcinosis
Renal: polyuria, kidney stones, hypercalciuria
Gastrointestinal: anorexia, nausea, vomiting, abdominal pain, constipation
Neuromuscular: proximal myopathy, weakness, fatigue, depression, inability to concentrate
Cardiovascular: hypertension, bradycardia, QT interval prolongation, left ventricular hypertrophy
pathophysiology of hyperparathyroidism
PTH is normally release during hypocalcemia
BoneIncreases RANKL expression and decreases OPG which results in an increase in bone resorption and an increase in plasma calcium and phosphate levels
In DCT, PTH stimulates the Ca2+/Na+ antiporter which results in an increase in Ca2+ reabsorptionIn PCT, PTH inhibits the Na+/phosphate symporter which results in an increase in phosphate secretion
IntestinesPTH increases intestinal absorption of Ca2+ and phosphate via the vit D pathway
Stimulates 1-OHase
Hypercalcemia causes many of the symptoms listed above (bones, stones, groans)
Hypophosphatemia causes bone pain, confusion and muscle weakness
treatments of hyperparathyroidism
goal to prevent secondary hyperparathyroidism, renal osteodystrophy, vascular and extravascular calcification
when nothing else works parathyroidectomy (causes hypocalcemia and hyperphosphatemia)
eat less phosphate (decrease release PTH) Meats, dairy products, nuts, peanut butter, beans, colas, & BEER contain phosphorus
phosphorus binding car (TUMS, sevlamer)
vitamon D supplements (increase calcium negative feedbacks PTH, hyperphosphoratemia can increase levels of PTH, so vitamon D therapy may not always be good)
cinacalcet (increases parathyroid receptors sensitivity to calcium which negative feedbacks PTH)
biphosphanates inhibit calcium loss from bones by inhibiting osteoclasts
parathyroid gland
anterior of the thyroid gland
not regulated by the hypothalamus or pituitary gland
hypoparathyroidism
low calcium
high phosphate
hypoparathyroidism in the bones
low PTH decreases osteoclast activity
decrease PTH binding-->decrease RANK expression-->increase OPG expression-->both decrease osteoclast activity-->decrease plasma Ca
hypoparathyroidism in intestines
decrease PTH-->decrease 25 hydroxyvitamin D3 1-alpha hydroxylase-->decrease active vitamin D-->decrease intestinal absorption of calcium
hypoparathyroidism in kidneys
decrease PTH-->decrease Na/Cl antiport, and increase in phosphate
signs and symptoms of hypoparathyroidism
1. Tingling burning (paresthesias)
2. Muscle aches or cramps affecting
3. Twitching or spasms of your muscles
4. Fatigue or weakness
5. Painful menstruation
6. Patchy hair loss
7. Dry, coarse skin
8. Brittle nails
9. Anxiety or nervousness
10. Headaches
11. Depression, mood swings
12. Memory problems
hypoparathyroidism lab results
Low Calcium
b. Low Parathyroid Hormone
c. High Phosphorous
d. Low Magnesium
e. Drugs may alter lab results (i.e. corticosteroids)
f. Disorders may alter lab results (other hormonal disorders; i.e. hypoalbuminuria)
2. ECG
a. Can detect arrhythmias associated with hypocalcemia
b. Increased Q-T
c. Increased S-T intervals
3. X-Rays & Bone Density Tests
a. Can determine if abnormal Ca++ levels have affected the strength of bones
b. In diagnosing children, doctors check to see whether tooth development is normal and whether they have met developmental milestones
diseases associated with hypoparathyroidism
Hereditary: chromosomal mutations
1. DiGeorge Syndrome
2. Kenny Caffey
3. Sanjad Sakati
B. Acquired: surgery results in accident partial or full parathyroidectomy
C. Transient: after surgery can have hypothyroisidism for a short period of time, goes back to normal
D. Idiopathic
E. Psuedohypoparathyroidism: Tissue is resistant to parathyroid hormone
hypoparathyroidism treatment
calcium and vit D supplements
PTH isn't approved by FDA
signs and symptoms of cushings symdrome
A. Fat distributed to the midsection (centripetal fat), moon face, buffalo hump, and thin limbs
B. Obesity with uncontrolled type 2 diabetes
C. In both animals and humans
cushing disease caused by long term exposure to cortisol pathophysiology
Glucocorticoid released from the adrenal glands
a. Hypothalamus releases corticotropin-releasing hormone (CRH) and antidiuretic hormone (ADH)--> anterior pituitary releases adrenocorticotropic hormone (ACTH) -->adrenal cortex releases cortisol
excess cortisol causes:
a. Extreme lipolysis- fat deposition in face and neck (buffalo hump) as well as around the trunk (centripetal fat)
b. Extreme proteolysis- thin limbs due to breakdown of muscle as well as striae due to a decrease in collagen fibers
cushing disease causes by the body producing to much cortisol pathophysiology
1. Pituitary gland tumor
a. Main cause of Cushing’s disease
b. Non-cancerous tumor on the pituitary gland
i. Excess ACTH is secreted from the pituitary gland  excess cortisol is released from the adrenal gland
2. Ectopic ACTH-secreting tumor
a. Rarely occurs
b. Cancerous or non-cancerous tumor that causes a tissue that does not usually secrete ACTH to start secreting ACTH
i. Excess ACTH  excess cortisol is released from the a adrenal gland
c. Typically find these tumors in the lungs, pancreas, thyroid, or thymus gland
3. Primary adrenal gland disease
a. Adrenal disorder that causes excess release of cortisol without ACTH stimulation
i. Excess cortisol  negative feedback onto anterior pituitary gland  extremely low amounts of ACTH
b. Adrenal adenoma
i. Most common type of adrenal disorder
ii. Non-cancerous tumor on the adrenal gland
c. Adrenocortical Carcinoma
i. Very rare
ii. Cancerous tumor of the adrenal gland
4. Familial Cushing’s Syndrome
a. Most causes are not inherited
b. Rarely, people can inherit the tendency to develop tumors
i. Inherited tumors could lead to excess cortisol production and eventually Cushing’s
cushing disease caused by exogenous excess of glucocorticoids
High levels of cortisol due to an external source
a. Taking corticosteroids for long periods of time (RA, immunosuppressant, implants)
i. Prednisone
ii. Methyprednisone
b. Oral or injected corticosteroids
i. Inhaled and topical corticosteroids usually given in too low of a does
testing for cushings disease
1. 24-hour urinary free cortisol level
a. Urine samples taken over a 24-hour period and tested for cortisol
i. Higher than 50-100 mcg = Cushing’s
2. Midnight plasma cortisol reading
a. Plasma level of cortisol read at midnight
b. Levels supposed to be low at night but not in Cushing’s
i. Higher than 50 nmol/L = Cushing’s
3. Low-dose dexamethasone suppression test (LDDST)
a. Low levels of Dexamethasone (synthetic glucocorticoid) given PO Q6H for 2 days
b. Urine tested before dose and multiple times during 2 days
c. Glucocorticoid negative feedback onto anterior pituitary  decreased levels of ACTH  decreased levels of cortisol
i. No decrease in cortisol levels = Cushing’s
4. Dexamethasone-corticotropin-releasing hormone (CRH) test
a. Injection of CRH pretreated with dexamethasone
b. Elevations of cortisol during this test suggest Cushing’s
testing for the cause of cushings disease
1. CRH stimulation test
a. Injection of CRH given to distinguish if cause is a pituitary adenoma (ACTH and cortisol levels will rise), an eptopic ACTH syndrome (rarely rise), or adrenal tumors (never rise)
2. High-dose dexamethasone suppression test (HDDST)
a. High dexamethasone levels decrease cortisol levels in healthy people but not if you have a ACTH-producing tumor
3. MRI/CT of endocrine glands
a. Help determine if a tumor is present
4. Petrosal sinus sampleing
a. ACTH levels in the petrosal sinus (veins that drain from the pituitary) are compared to those of a forearm vein
i. Higher ACTH levels in the petrosal sinus indicate pituitary adenoma
treatment for cushings disease
A. Surgical Treatment
1. Pituitary Adenoma (ACTH secreting)
a. Transsphenoidal tumor resection- surgical procedure through which the pituitary adenoma is removed through the nose
i. Has the highest efficacy – 98%
b. Bilateral adrenalectomy- removal of the adrenal gland(s) to prevent ACTH stimulation of cortisol production
i. Last resort!
2. Ectopic Adenoma (ACTH secreting)
a. Tumor removal if the tumor can be found. Radiation therapy or pharmacologic therapy is a secondary option
3. Adrenal Adenoma (cortisol/aldosterone secreting)
a. Surgical resection of the adenoma- patient given glucocorticoids before and after removal to stabilize cortisol levels
B. Pharmacological Trealments
1. Ketoconazole- acts as an antagonist for cholesterol desmolase by blocking the action of the ATCH. Cholesterol desmolase activates the first step of cortisol synthesis from cholesterol. It also antagonizes both aldosterone and adrogen synthesis.
2. Spironolactone- Antagonizes aldosterone synthesis and restores normal potassium levels, which helps to lower blood pressure
C. Iatrogenic Treatment- treats Cushing’s that is due to glucocorticoid therapy.
1. This is the most common cause of Cushing’s Syndrome
2. Absolutely essential to slowly decrease the dose of glucocorticoids because of atrophied adrenal glands. If glucocorticoid treatment is immediately stopped, there is a risk of cortisol levels suddenly dropping to dangerously low levels.
etiology of addisons disease
Typical presentation is adults between 30 and 50 years old
adrenal hormones secreted by the adrenal cortex
Cortisol
Glucocorticoid that stimulates the breakdown of fat and protein for gluconeogenesis
Secretion is regulated by adrenocorticotropic hormone (ACTH)
ACTH secretion is regulated by hypothalamic corticotropin-releasing
Hormone (CRH) –and vasopressin
ACTH is regulated in 3 ways: episodic bursts/diurnal (circadian) rhythym, stress response, negative feedback
Aldosterone
Primary function to regulate Na+ excretion and maintain normal intravascular volume
-Regulated by the rennin-angiotensin system, ACTH, and plasma electrolytes (K+ and Na+)
Increases the amount and activity of sodium channels
Androgens
Addison’s Disease (Primary Adrenal Insufficiency)
Is Primary adrenocortical insufficiency – caused by destruction or dysfunction of the adrenal cortex Destruction of the adrenal cortex results in decreased adrenal glucocorticoid reserve.
At first basal glucocorticoid secretion is normal but no response to stress/trauma
Further loss of cortical tissue will cause loss of basal secretion of glucocorticoids and mineralocorticoids become deficient.
With the fall in plasma cortisol, reduction of the negative feedback of pituitary ACTH secretion and increased levels of ACTH
Secondary Adrenocortical Insufficiency (a deficiency of pituitary ACTH or hypothalamic CRH)
Occurs when large doses of glucocorticoids are given for anti-inflammatory and immunosuppressive effects.
When treatment lasts longer than 4-5 weeks there is prolonged suppression of CRH, ACTH, and endongenous cortisol secretion.
If treatment is abruptly stopped, the hypothalamus and pituitary will not respond to the lack of cortisol and therefore insufficiency ensues.
Both primary and secondary insufficiency result in decreased levels of glucocorticoid, mineralocorticoid and Androgens
Causes of Addison’s Disease
Autoimmune Destruction (80% of cases)
related to generation of antiadrenal antibodies
can be either isolated or associated with other autoimmune disorders
the types of antibodies produced are either adrenal cortex antibodies (ACA) or antibodies to the steroid 21-hydroxylase enzyme (cytochrome P450c21)
Tuberculosis (~20% of cases)
causes adrenal failure or near total destruction of both glands
results from the spread of systemic infection to the adrenal cortex
adrenal tissue is destroyed and is replaced with caseous necrosis
AIDS related adrenalitis
occurs in the late stages of HIV infection
adrenal gland is affected by opportunistic infections
many patients with AIDS have necrotizing adrenalitis, but only 50-70% of the gland is destroyed so not Addison’s
Other (hemorrhage, metastases, genetic disorders)
How does adrenal insufficiency affect the body?
Cortisol deficiency
Impaired gluconeogenesis predisposes to hypoglycemia during fasting
Hypersecretion of ACTH increases Melanocyte Stimulating Hormone resulting in hyperpigmentation of skin, nail beds, pressure points, and can cause scars. (only in primary insufficiency)
Aldosterone deficiency
Hypovolemia and hyperkalemia due to renal loss of Na+ and retention of K+
Excess release of vasopressin
Inability to excrete water load leading to hyponatremia
Low GFR
signs and symptoms of addisons disease
Hyperpigmentation of skin and mucous membranes due to accumulation of ACTH which stimulates melanocytes to produce melanin
Craving for Salt or salty food due to urinary loss of sodium
Orthostatic hypotension – low blood pressure that falls further when standing
Nausea, vomiting
History of Amenorrhea in female patients
Adrenal or Addisonian Crisis
Symptoms include: sudden pain in lower back, abdomen or lower leg, low blood pressure, temperature reaching 105 or greater, severe lethargy, comatose, syncope, shock, and death
Diagnosis of Addison’s Disease
Blood tests
Sodium, Potassium, Cortisol and ACTH serum levels
Assay antibodies to test for autoimmune disease
ACTH stimulation test (injection of synthetic ACTH)
cortisol levels are measured before and after injection
patients with Addison’s or long-standing secondary adrenal insufficiency will show little if any response
May test at low and high doses of ACTH to determine degree of atrophy in secondary insufficiency
CRH stimulation test (synthetic CRH injection used when ACTH test response is abnormal)
Can help determine the cause of adrenal insufficiency
Blood cortisol is measured before and, periodically, after the injection.
Patients with Addison’s disease produce high levels of ACTH but no cortisol.
2o insufficiency shows absent or delayed ACTH responses.
An absent ACTH response points to the pituitary
A delayed ACTH response points to the hypothalamus
Insulin-induced hypoglycemia test (insulin injection)
Usually called for if pituitary gland disease is expected
Test blood sugar and cortisol levels at various points after injection
Normally, glucose levels fall and cortisol levels rise after injection
Post-Diagnosis Assessments
X ray or Ultrasound of the abdomen
Used to check  adrenals for signs of calcium deposits
Calcium deposits may indicate bleeding or TB
Tuberculin skin test may be used to rule out TB
(CT) scans can check size of adrenal or pituitary gland for atrophy
Emergency Situations
measure serum ACTH and cortisol (before glucocorticoids are given)
enough to make preliminary diagnosis
Treatment of Addison’s Disease
First line treatment is corticosteroid replacement therapy via oral tablets (hydrocortisone, prednisone or cortisone acetate are used prevalently).
Aldosterone is replaced by fludrocortisone.
An androgen replacement (dehydroepiandrosterone) improves their mood and sex drive in some women
Treatment of an addisonian crisis typically consists of IV hydrocortisone, saline and dextrose that restores blood pressure, sugar and potassium levels
functional anatomy of male reproductive system
sperm: produced in seminiferous tubules (900 of these in testies)
travels from seminiferous-->epidymis-->vasdeferens-->ejaculary duct-->urethra
glands that also secrete stuff into sperm: prostate, seminal vesicles, bulbourethral (cowper's gland)
younge to old-->spermatagonia production-->undergo meiosis in peuberty by FSH and LH secretion to become sperm
describe the steps in spermatogenesis
spermatagonia migrate to central lumin of seminiferous tubules and are surrounded by nourashing sertoli cells-->divide into speratocytes (diploid)-->divide into spermatids (haploid)-->elongate into spermatozoa (develope head and tail) (head has chromosomes and acrosome (enzymes (Hyaluronidase and proteases necessary for egg penetration))) (tail is flagelem)
takes around 74 days
describe the actions of hormones involved in spermatogensis
testosterone (secreted from interstitial leydig cells (located near seminiferous tubules)) growth of spermatagonia at first stages

LH (secreted from anterior pituitary) (stimulated by GnRH) stimulate leydig cells to produce testosterone

FSH (secreted from anterior pituitary) (stimulated by GnRH from hypothalamus) activate sertoli cells to change spermatids-->sperm

estrogens (secreted by sertoli cells (stimulated by FSH)) final stages of spermatogenesis

GH: maintains metabolic environment (without GH (dwarfs) infertility results)
explain sperm maturing and storage
seminiferous tubules-->epididymus (gain movement)-->e

Must have alkaline environment

Storage at slightly lower temperatures

stored in vas deferens or epididymus (good for 1 month)
explain egg penetration
penetrate the corona radiata composed of granulosa cells-->zona pallucida-->binding and acrosomal membrane deterioration-->egg and sperm fuse (takes 30 min) (only one sperm can fuse (unknown mechanism))
explain male erection and orgasm
PNS release NO-->dialates arteries (primarily corpus cavulosum)

female PNS secretes vaginal lubrication

ejaculation: contraction of vas deferens and urethra (stimulated by SNS)-->eject semen
other sperm secretions
during ejaculation (sertoli cells secrete testosterone, estrogens, enzymes and nutrients essential for maturation)

after sperm seminal vesicles secrete a mucoid fluid containing fructose, citric acid and other nutrients plus significant quantities of PG’s ( helps in the uterus and fallopian tubes so helping the sperm reach the eggaid sperm movement and penetration plus causing reverse peristaltic waves) and fibrinogen

prostate gland: secretes Ca, citrate, phosphate, clotting factor, profibrinolysin (increases PH)

clotting factor and fibrinogen causes coagulation to hold sperm in vagina for 15-30 minutes-->after 15-30 minutes fibrinolysin dissolves semon
explain capacitation, and activation
stops sperm from becoming active until inside the vagina

in the vagina inhibitory factors are washed away

acrosomal membrane is weakened in vagina due to less cholesterol

in vagina Ca permiability increases flagella motility-->run into walls needing acrosomal lyse enzymes-->weakened acrosomal membrane
describe abnormal spermatogensis
damaged seminiferous tubes

bilateral orchitis (testicular infection) (caused by mumps, scarlet fever, and pneumonia)

chiptochidism (testies don't descend into scrotum) (temp is too high) (may be caused by bad testosterone secretion)

sperm decreases by to 20 x 10^6 than infertile
what helps laydig cells secrete testosterone in fetel testies
placenta secrete human chorionic gonadotropin
why does the GnRH not release any sex hormones during childhood
pituititary gland is extremely sensitive to testosterone feedback

at peuberty this changes (unknown mechanism)
explain testosterone secretion
secreted by testies (leydig cells)

dihydrotestosterone is most active form

testosterone is an androgen

androgens are any hormone that has masculinizing effects

bound to beta-globullin-sex-binding-globullin

changed to dihydrotestosterone in target cells, but still needs some testosterone to work

any unbound metabolized in the liver to be secreted in bile and urine

probably changed to estrogen in sertoli cells in limited quantities

converted to dihydrotestosterone by 5alpha-reductase-->hits intracellular receptors-->effects transcriptions
explain sex determination
Y cromosome has SRY gene-->expressed 7th week of pregnancies-->for testies-->testosterone secreted from testies leydig cells-->wolffian ducts form into testies-->dihydrotestosterone stimulate penis, prostate, and scrotum development

in females sertoli cells secrete mullerian-inhibiting substance MIS (also no testosterone)--> female reproductive organs created
explain testosterone effects during pueberty
growth of penis, scrotum, and testies

pubic hair, chest hair

hypertrophy of larnyx (deepens voice)

thickining of skin, increased oil secretions

skeletal muscle building, bone growth

increasede metabolism

increase blood and ECF
problems with prostate with old age
fibrinadenomas
malignant cancers (stimulated by testosterone, inhibited by estrogens)
explain hypogonadism
testies doesn't secrete tesosterone
what is complete androgen insensitivity syndrome
hypothalamus doesn't secrete GnRH
what effects do testicular tumours in the leydig cells cause
increased testosterone: decreased height, increased skeletel muscle and sexual organ size
effects of tumors of germinal epithelium
sometimes secrete large amounts of hCG (acts like LH)

sometimes secrete large amounts of estrogens causing gynocomastia
explain the effects of pineal glands on sexual function
melatonin secretion of pineal gland may inhibit LH and FSH secretion
explain oogensis steps
cycle usually 28 days

FSH and LH (act via G-->AC-->cAMP) begin to be secreted during pueberty

granulosa cells of follicles secrete oocyte-maturation-inhibiting-factor

primary oocyte-->secondary oocyte-->ovum(2nd to ovum occurs after fertilization)-->primordial follicle-->primary follicle-->preantral follicle (antrum develops)-->early antral follicle-->mature follicle

1st days of cycle: FSH and LH cause 6-10 primary follicles to mature (2 layers of mature follicles(theca externa(connective tissue), theca interna(secrete progesterone and estrogen)))

several days into cycle: FSH stimulates folicles to secrete estrogen-->antrum devolops, granulosa cells upregulate FSH and LH receptors.
Increase estrogen and LH secretion stimulates thecal cell secretion-->increases egg size

1 week: One egg outgrows another: May be due to increased estrogen secretion by large cell inhibiting FSH secretion
explain ovulation steps
12th day: LH surge (may be caused by estrogen positive feedback instead of negative feedback, or granulosa cells increase progesterone secretion), FSH increase as well (both increase egg size) (LH stimulates granulosa cells to secrete progesterone and decrease estrogen)

14th day: outer wall swells (stigma)-->bursts (releases egg and granulosa cells) (corona radiate)

after ovulation corpus luteum secretes lots of estrogen, progesteron, and inhibit (lowest levels of LH and FSH (lasts 2-3 days before menstration))
explain regulation of menstal cycle
GnRH secretes LH and FSH in bursts every 1-2 hours

hypothalmic nuclei stimulated by the lymbic system regulate sexual function

estrogen or estrogen with progesterone inhibit FSH and LH secretion most, and GnRH secretion a little less

inhibit is secreted by granulosa cells and inhibits FSH mostly and LH a little less
explain menstration steps
after LH and FSH are at smallest levels, estrogen, progesterone, and inhibin stop feedback, follicular cells grow, LH and FSH levels rise-->increased estrogen secretion by granulosa cells-->estrogen might start positive feedback again
explain the ovarian hormones
estrogen: (non-pregnants): secreted by ovaries: 3 estrogens (b-estrodiol(far more potent than others), estrone, estriol)

Progesterone: secreted by corpus luteum after ovulation

progesterone and testosterone secreted, but almost all is changed into estrogens by corpus luteum (after ovulation so much progesterone is secreted that it isn't changed)

estrogens and progesterone both bound to albumin and plasma-globullins

estrogens metabolized by liver by conjugation or changed to estriol (virtually inactive)

progesterone metabolized into pregnanediol (inactive) and secreted
explain the function of estrogens
changes vaginal epithelium cubiodal-->stratified ciliated(helps trauma and infections)

fallopean tubes changed to statified cilliated

breasts: (also requires progesterone, prolactin, oxytocin, etc.) stromal tissue, ductile system growth, fat deposition

increase growth a little bit (less estrogen causes osteoporosis)

weak protein formation, week sex organ development, fat deposition

retain a little water during menstration (similar in structure to aldosterone)
functions of progesterones
secretory changes in uterine endometrium after ovulation to prepare for implantation

decreases uterine contractions to stop expulsion of the egg

increase secretion of fallopean tubes to nourish eggs

breast development
explain menstral cycle steps
1st step: increased estrogen causes regrowth of endometrium (proliferative phase)

2nd step: glands in cervix secretes mucus to help incoming sperm

3rd step: Ovulation (follicle bursts)

4th step: after ovulation estrogen and progesterone from corpus luteum stimulate nutrient secretion in the endometrium to help any fertilized eggs (7-9 days after ovulation)(secretory stage)

5th step: if fertilization doesn't occur corpus luteum degrands, estrogen and progesterone decreases-->triggers menstration

6th step: endometrium is expelled in urin with blood and tissue fluid-->WBC come in to prevent infection during menstration
what initiates peuberty
increased LH and FSH
describe menopause
40-50 years old cycles become irregular

no ovaries-->low estrogen secretion-->increased FSH and LH

decreased estrogen causes:
hot flashes
dypsnea
irritability
fatigue
anxiety
phycosis
decreased bone and muscle strength
describe some abnormalities in ovary secretion
hypogonadism: low secretion of sex steriods-->poorly developed ovaries

(before puberty sexual organs not developed, and tall because epiphyseal plates don't fuse)

after puberty similar results to menopause

hypersecretion: limited by negative feedback

caused maybe by a tumour of the granulosa cells

causes irregular bleeding
describe the female orgasm
tighting of the vagina

increase mucous secretions

increase uterine and fallopean tube motility

dialation of cervical canal

secretion of oxytocin

rythmic contraction of the uterus
what is the female fertility window
ovum only stays good 24h after ovulation

sperm stays good for 5 days.
How does birth control work
secrets estrogen to prevent LH surge prior to ovulation
what are some problems with women fertility
lack of ovulation: helped by hCH (mimics LH)

endometriosis: endometrium grows too much

salpingitis: inflamation of the falopean tubes

abnormal cervix mucus secretion can decrease sperm motility
what are the classifications for hypothyroidism
primary: thyroid
secondary: anterior pituitary
tertiary: hypothalamus
describe primary hypothyroidism in children
without TH babies will become in infants:

retarted, unless thyroxin is given immediatly after birth

caused by iodine defecancy in women

as baby grows, insufficiant thryroid hormone leads to cretinism: mental retardation and stunted growth
types of primary hypothyroidism
acute thyroiditis: bacterial infection (enlarged tender thyroid, fever)

subacute thyroiditis: non bacterial infection (maybe after viral infection) enlarged, tender thyroid, tenderness

autoimmune thyroiditis: Hashimoto disease, chronic lymphocytic thyroiditis: destruction of thyroid by antibodies and/or lymphocytes

may be associated with a goiter
signs and symptoms of hypothyroidism
weight gain
low energy
cognitive dysfunction
thin, brittle hair, brittle fingernails
dyspnea upon exertion
myxedema: hypotension, bradycardia, mental impairdness, multisystem organ failure
pathophysiology of primary hypothyroidism
often autoimmune destruction of thyroid peroxidase and thyroglobulin (stops iodination, organofaction, MIT and DIT binding)

Also caused by excess iodine (treated with amiodarone, KI, and other iodine contianing drugs)

thyroiditis: inflamation of thyroid also causes problems
pathophysiology of secondary hypothyroidism
decreased secretion of TSH

caused by tumor, radiation, or inflamation
pathophysiology of tertiary hypothyroidism
decreased TRH secretion by hypothalamus
origin of TSHR antibody (graves disease)
genetically linked

viral antigen similar to TSH receptor
effect of hyperthyroidism on the heart
increased b receptors

increased catacholamines

increase HR/contractility/CO

decreased a receptor (vascular dialation)
effects of hyperthyroidism in the eyes
exophthalmus/proptosis: increased sympathetic tone. build up lympocytes, mucopolysaccarides, and edema fluid
treatment of hyperthyroidism
antithyroid drugs (methimazole MMI, propylthiouracil PTU)

radioactive iodine:
most common
kills part of the thyroid

surgical removal of thyroid
fuzing egg and sperm to 8 weeks
1st: in fallopean tube for 3 days (isthmus contracts and prevents it)

2nd. increased progesterone by corpus luteum causes relaxation of isthmus, and the egg moves to uterus

3rd. delayed in the uterus 3 days to complete nurousing environment

4th. implantation: trophoblast cells secrete proteolytic enzymes that allow connection with endometrium

5th. cells divide to form baby beginings and placenta

6th. corpus luteum provides nuroushment until 8 weeks when placenta is fully developed
explain the placenta
trophoblastic cells grow into endometrium-->capillaries grow out of baby(16 days after fertilization a heart beats)-->blood sinus from mother grow around these chords(placental villi)-->blood comes from mother via 2 arteries, leaves via 1 vein(fetal blood has 50% more Hb/vol)(leaving co2 of baby is acidic(shifts mothers curve to right(releases more O2 to baby)))(alkaline baby blood take mother's O2)-->FA's are simple diffused, glucose amino acid are facilitated diffusion-->
decribe the major hormones of pregnancy
placenta secretes:hCG, estrogens, progesterone and Human Chorionic Somatomammotropin

hCG: secreted by trophoblasts
stimulates secretion of sex steroids (prevent menstration, helps endometreum grow)
maintains corpus luteum
in males hCG stimulates testies to secrete testosterone

after 12 weeks of pregnancy corpus luteum is finished

estrogens: growth of sex organs

progesterone:
devolopes decidual cells (involved in fetal nutrician)
inhibits uterine contractility to prevent abortion
works with estrogen for breast devolopment

hCS:
not clearly understood
acts like GH by decreaseing insulin sensitivity (allows glucose to be available to the baby)
breast development
milk production
explain hormones activity that are indirectly affected by pregnancy
affected due to increased metabolism and pregnancy hormones

anterior pituitary enlarges: secretes increase ATCH, TSH, and prolactin

thyroid gland enlarges: secretes more thyroid hormones
due to placental secretion of hCT, and hCG

parathyroid enlarges (especially if the mother has low Ca diet)
baby needs Ca for bones and Ca for milk

aldosterone is increased, causes bloating and sometimes hypertension

Relaxin
secreted by corpus luteum
stimulated by hCG
relaxes symphsis tendens in birth canal to allow baby to come out(estrogens are however more important than relaxin in this mechanism)
responses of the mother to pregnancy
edema
acne
increased size of sex organs
masculinity of features sometimes

24 lbs is usually gained during pregnancy. (7lb for baby, 4lb for fluids, 13lb for fat)

nutrician is most demanding in last trimester

last trimester has increased blood demand, so CO of mother is increased

blood volume increase 30% to help baby, and blood loss during pregnancy

O2 demand/CO2 voiding increases near end of pregnancy

progesterone increases sensitivity to pCO2 chemosensitive area
what is preclamsia and eclamsia
hypertension and protein in urine during last few weeks of pregnancy

preclamsia<eclamsia

eclamsia can be deadly

treated with vasodialators and immediate delivory
describe the onset of labor
frequency and intensity of contractions (braxton hicks contractions) increase until maxed out at pregnancy

mechanism unknown, but maybe positive feedback by cervix stretching

labour causes pain, which causes abdominal muscles to contract and expel the baby

10-14 min after birth uterus shrinks expeling placenta and blood
describe what happens right before birth
progesterone decreases contractility of birth canal
estrogen increases contractility by increases gap junctions and coupaling

as birth approaches estrogen increases, progesterone levels out


oxytocin during birth:
progesterone decreases contracility of birth canal

estrogen increases contractility by increases gap junctions and coupaling

as birth approaches estrogen increases, progesterone levels out


as birth approches, body upregulates oxytocin receptors
oxytocin increases during birth

stretch receptors cause smooth muscle contractions durng birth by babies head hitting cervix
lactation
many hormones effect lactation (estrogen from the placenta plus GH, prolactin, cortisol, insulin and PTH) progesterone does the most however

after birth progesterone and estrogen decrease allowing prolactine to start production of milk

milk suckling produces a surge of prolactin which makes milk for next feeding

oxytocin causes milk letdown by contracting myoepithelial cells around milk glands (stimulated by suckling)

prolactin secretion may inhibit GnRH secretion by hypothalamus which inhibits LH and FSH