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255 Cards in this Set
- Front
- Back
acute renal failure defnition
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decline in renal function within 24-48 hours
|
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acute renal failure symptoms
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reduced GFR
decreased urine output azotemia (uremia) |
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Azotemia (Uremia)?
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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 |
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common causes of chronic renal failure
|
diabetes
hypertension glomerulonephritis polycystic kidney disease |
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is chronic renal disease reversable
|
no
|
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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 |
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what are the two compensetory mechanisms in renal disease that lead to increased GFR
|
more prosteglandins: afferent vasodialation
angiotensin II: efferent vasoconstriction |
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stage 1 numbers
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> 90ml/min
|
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stage 2 numbers
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60-90ml/min
|
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endocrine glands are what tissue
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epithelial
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endocrine glands secret into what
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blood stream
|
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what are neuroendocrine cells
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neurons that secret stuff into blood stream
|
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the release of peptides are similar to what type of release in neurons
|
ca mediated exocytosis
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how many ca domains are their in neuroendocrine cells
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one
|
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do neuroendocrine cells constantly need activation to release peptides by ca
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no, some peptides are perminatly activated by ca
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do hormones affect take place at the same pace
|
no, growth hormones for example are slow, adrenaline for example is fast
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do hormone receptors have high or low affinity for hormones
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very high
|
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which type of hormones are bound to plasma proteins
|
steroids and thyroid hormones
|
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what is the metabolic clearance rate
|
rate of clearnace of hormone/concentration of hormones in plasma
|
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how are hormones cleared
|
metabolism
tissue binding excretion of bile urine |
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leptin
|
adipose tissue
appetite, metabolism, reproduction |
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cortisol
|
adrenal cortex
metabolism stress immune system devolopment |
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androgens
|
adrenal cortex
sex drive in women menstration |
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aldosterone
|
adrenal cortex
na/k secretion in kidneys |
|
epinephrine
norepinephrine |
adrenal medula
metabolism cardiovascular function |
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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 |
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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) |
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what is the interface between neuron and endocrine system
|
hypothalumus
|
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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) |
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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) |
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PTH regulates what
|
calcium and phosphate in the GI, renal secretion, and bone exchange
|
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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
|
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kidneys does what to PTH
|
secretes it rapidly, but does not secrete its fragments which cause its effects
|
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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%
|
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peak age of those with kidney stones
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20-50 years old
|
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what kind of kidney stones are with men
|
calcium oxalate
urate and cystine (with both) |
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what kind of kidney stones are with women
|
struvite
urate and cystine (with both men and women) |
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what causes symptoms from kidney stone
|
if above the pelvis no symptoms
problems when it is in the ureter and prevents dranage |
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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 |
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life style changes when you have a kidney stone
|
increase fluids (water is best)
eat less calcium, vit D, etc. |
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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
|
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long term catheter will cause what infection
|
UTI
|
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what are risk factors for male UTI's
|
old
|
|
lower uti symptoms
|
dysuria
painful urination frequent urges to urinate suprapubic heaviness nocturia |
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upper uti symptoms
|
flank pain
fever nasea malaise |
|
asystematic UTI's occur in what people group
|
old people
|
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what is a complicated UTI
|
one with a
lesion, stone, or other block male infections indwelling catheter prostatic hypertrophy |
|
upper UTI located where
|
kidneys
|
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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
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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 |
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hypoparathyroidism treatment
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calcium and vit D supplements
PTH isn't approved by FDA |
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signs and symptoms of cushings symdrome
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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 |
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cushing disease caused by long term exposure to cortisol pathophysiology
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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 |
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cushing disease causes by the body producing to much cortisol pathophysiology
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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 |
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cushing disease caused by exogenous excess of glucocorticoids
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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 |
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testing for cushings disease
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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 |
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testing for the cause of cushings disease
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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 |
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treatment for cushings disease
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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. |
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etiology of addisons disease
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Typical presentation is adults between 30 and 50 years old
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adrenal hormones secreted by the adrenal cortex
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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 |
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Addison’s Disease (Primary Adrenal Insufficiency)
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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 |
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Secondary Adrenocortical Insufficiency (a deficiency of pituitary ACTH or hypothalamic CRH)
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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 |
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Causes of Addison’s Disease
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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) |
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How does adrenal insufficiency affect the body?
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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 |
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signs and symptoms of addisons disease
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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 |
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Adrenal or Addisonian Crisis
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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
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Diagnosis of Addison’s Disease
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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 |
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Treatment of Addison’s Disease
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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 |
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functional anatomy of male reproductive system
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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 |
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describe the steps in spermatogenesis
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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 |
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describe the actions of hormones involved in spermatogensis
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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) |
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explain sperm maturing and storage
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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) |
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explain egg penetration
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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))
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explain male erection and orgasm
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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 |
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other sperm secretions
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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 |
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explain capacitation, and activation
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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 |
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describe abnormal spermatogensis
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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 |
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what helps laydig cells secrete testosterone in fetel testies
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placenta secrete human chorionic gonadotropin
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why does the GnRH not release any sex hormones during childhood
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pituititary gland is extremely sensitive to testosterone feedback
at peuberty this changes (unknown mechanism) |
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explain testosterone secretion
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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 |
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explain sex determination
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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 |
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explain testosterone effects during pueberty
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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 |
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problems with prostate with old age
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fibrinadenomas
malignant cancers (stimulated by testosterone, inhibited by estrogens) |
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explain hypogonadism
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testies doesn't secrete tesosterone
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what is complete androgen insensitivity syndrome
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hypothalamus doesn't secrete GnRH
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what effects do testicular tumours in the leydig cells cause
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increased testosterone: decreased height, increased skeletel muscle and sexual organ size
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effects of tumors of germinal epithelium
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sometimes secrete large amounts of hCG (acts like LH)
sometimes secrete large amounts of estrogens causing gynocomastia |
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explain the effects of pineal glands on sexual function
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melatonin secretion of pineal gland may inhibit LH and FSH secretion
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explain oogensis steps
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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 |
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explain ovulation steps
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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)) |
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explain regulation of menstal cycle
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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 |
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explain menstration steps
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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
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explain the ovarian hormones
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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 |
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explain the function of estrogens
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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) |
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functions of progesterones
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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 |
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explain menstral cycle steps
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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 |
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what initiates peuberty
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increased LH and FSH
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describe menopause
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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 |
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describe some abnormalities in ovary secretion
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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 |
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describe the female orgasm
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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 |
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what is the female fertility window
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ovum only stays good 24h after ovulation
sperm stays good for 5 days. |
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How does birth control work
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secrets estrogen to prevent LH surge prior to ovulation
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what are some problems with women fertility
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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 |
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what are the classifications for hypothyroidism
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primary: thyroid
secondary: anterior pituitary tertiary: hypothalamus |
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describe primary hypothyroidism in children
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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 |
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types of primary hypothyroidism
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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 |
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signs and symptoms of hypothyroidism
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weight gain
low energy cognitive dysfunction thin, brittle hair, brittle fingernails dyspnea upon exertion myxedema: hypotension, bradycardia, mental impairdness, multisystem organ failure |
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pathophysiology of primary hypothyroidism
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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 |
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pathophysiology of secondary hypothyroidism
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decreased secretion of TSH
caused by tumor, radiation, or inflamation |
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pathophysiology of tertiary hypothyroidism
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decreased TRH secretion by hypothalamus
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origin of TSHR antibody (graves disease)
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genetically linked
viral antigen similar to TSH receptor |
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effect of hyperthyroidism on the heart
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increased b receptors
increased catacholamines increase HR/contractility/CO decreased a receptor (vascular dialation) |
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effects of hyperthyroidism in the eyes
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exophthalmus/proptosis: increased sympathetic tone. build up lympocytes, mucopolysaccarides, and edema fluid
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treatment of hyperthyroidism
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antithyroid drugs (methimazole MMI, propylthiouracil PTU)
radioactive iodine: most common kills part of the thyroid surgical removal of thyroid |
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fuzing egg and sperm to 8 weeks
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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 |
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explain the placenta
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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-->
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decribe the major hormones of pregnancy
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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 |
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explain hormones activity that are indirectly affected by pregnancy
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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) |
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responses of the mother to pregnancy
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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 |
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what is preclamsia and eclamsia
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hypertension and protein in urine during last few weeks of pregnancy
preclamsia<eclamsia eclamsia can be deadly treated with vasodialators and immediate delivory |
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describe the onset of labor
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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 |
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describe what happens right before birth
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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 |
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lactation
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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 |