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function of LH
stimulates laydig cells to produce testosterone
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function of FSH
spermatogenesis
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function of inhibin
- stops spermatogenesis
- inhibits FSH
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testosterone as a metabolite
- dihydrotestosertone- 5-alpha-reductase
- estridiole- aromatase
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sertoli cells vs. leydig cells
- sertoli cells- testosterone r/c for spermatogenesis, FSH receptor, nurses sperm
- leydig cells- absent during childhood, LH receptors to make testosterone
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hormones influencing spermatogenesis
testosterone, inhibin, and FSH
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erection vs. ejaculation
point (parasymp) and shoot (symp)
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semen- fibrinolysis and clotting enzymes
plug the uterus to the dont fall out! then loosens back up so they can swim
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gonadotropin production over a lifespan- LH vs FSH
- fetus- high FSH
- adult- high LH
- old- high FSH
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function of mullerian inhibiting hormone
allow male development
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diabetic neuropathy:
c-peptide deficiency in type 1 diabetes
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if patiend has high blood glucose but UA is negative for ketones:
type 2
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role of glucagon
- hyperglycemic, increased blood glucose
- made by alpha cells
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role of somatostatin
- make by delta cells
- inhibits glucagon and insulin causing increased blood glucose time in the blood
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IDDM vs NIDDM
- IDDM= type 1, no insulin secretion, ketones
- NIDDM= type 2, insulin r/c desensitization, no ketones
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why cardiovascular disease with DM?
CHOL deposited in blood vessles
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lack of insulin- protein
protein wasting-> AA -> blood
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polyol pathway
- stimulated in high blood glucose
- attaches glucose to protiens
- causes cross-linking= malfunction
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24 year old swimmer presents with chronic back pain
extreme fatigue after practive and muscle weakness. reports increaed urination but also very thirsty. weight loss above 20 lbs in 1 month and wasnt trying. blury vision
bp 110/70, pulse 60, respiration 22, decreased grip strength
type 1 DM
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labs show positive ketones and glucose, low specific gravity.
Fasting glucose >300
type 1 DM
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30 year old overweight female with chronic back pain.
increased weight, irregular menses, cant get pregnant, poor diet.
BMI= 34.3, BP 140/90, pulse 75, respiration 16, truncal obesity, hirsuitism noted chin, facial acne
type 2 DM
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hormones that cause hyerglycemia
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hormones that cause hypoglycemia
insulin
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stimulation of beta cells
glucose, Ca++
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insulin actions on CHO- liver
- increase glycogen synthase
- decrease glycogen phosphorylase
- STORAGE!
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insulin actions on CHO- muscle
storage
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insulin actions on fat
storage, inhibits glycolysis
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insulin actions on protein
- storage as AAs
- increase protein synthesis
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class of insulin receptor? how does this lead to its function?
- enzyme linked
- phosphorylates glycogen
- Fast!
- transcription factors- slow
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38 year old with back pain. weakness in legs, truncal weight gain.
headache every day, increasing intensity.
overweight, irregular menses. BP= 160/90. purple stria on flanks, acne on face and back
cushings disease
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above patient has RA and has been taking steroids to maintain symptoms...still cushings disease??
- NO, CUSHINGS SYNDROME!!!!
- no tumor
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35 year old with headaches over past 6 months
heart palpatations, intense anxiety and panic attacks, lost over 30 lbs in 3 months. BP 190/100, pulse 120 and irregular. face is pale.
- medulla tumor of chromaffin cells
- -increased norepi and epi
need to make sure its not hyperthyroidism
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64 year old with increasing hirsutism. increasing fatigability, left-sided abdominal pain. deeper voice, no weight loss. blood pressure 200/110
tumor of adrenal reticularis causing too much androgen production
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a patient presents with alkalosis, hypertension and hyperglycemia. which hormone binds to which receptor to cause this?
cortisol binding to aldosterone r/c
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role of ACTH in aldosterone production
- maintains cholesterol synthesis in zona glomerulosa
- minor aldosterone regulation
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role of ANP in aldosterone
regulation of blood pressure by inhibiting aldosterone
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role of K and aldosterone
increase [K] stimulates aldosterone
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regarding cortisol and inflammation, which one doesnt belong?
decreases leukotrienes
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cellular stimulation by cortisol
cytoplasma to nucleus
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cortisol as diabetogenic hormone
- antagonize insulin r/c
- desensitized
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why does cortisol have mineralocorticoid activity?
simular to aldosterone
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if a patient presents with Cushings and is hypergimented, what is the source of excess cortisol and why
anterior pituitary tumor-> ACTH over stimulation
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