Module 6 - Endocrine system Flashcards
(142 cards)
1
Q
Def: endocrine system
A
Body system which uses hormones to communicate and send messages.
regulated byt NEGATIVE feedback loops
2
Q
Some Endocrine glands
A
*Hypothalamus
*Pituitary
Thyroid and parathyroid Glands
Adrenal Glands
Pancreas
Ovaries / Testes
3
Q
Exocrine function of the pancreas?
A
Secretes digestive enzymes directly into the GI tract
4
Q
Endocrine function of the pancreas?
A
Secretes hormones from the islets of langerhans
insulin - from Beta cells
Glucagon - from Alpha cells
5
Q
what is released in response to HIGH blood sugar?
*what is its job?
A
Insulin
- promotes the uptake, utilization and storage of glucose –> lowers blood glucose concentration
6
Q
what is released in response to LOW blood sugar?
*what is its job?
A
Glucagon
- increases the hepatic glucose glucose output –> increased blood glucose concentration
7
Q
what is Glycogen?
A
Stored Glucose.
8
Q
MOA: insulin
A
“the storage hormone” - promotes anabolism and inhibits catabolism of carbohydrates, fatty acids, and proteins
- suppresses endogenous glucose
- inhibits glucagon release
- causes rapid uptake, storage and use of glucose by insulin sensitive tissue - muscle, liver, adipose, brain
9
Q
usual amount of Insulin secreted in a day
A
25-50 units
10
Q
basal release rate of insulin
A
0.5-1.0 units/hour
11
Q
when would the rate of insulin release increase?
A
when blood glucose levels are >5.5mmol/L (in response to eating)
12
Q
beta cells secrete small amounts of insulin throughout the day?
A
Basal insulin release
13
Q
At meal times, insulin is rapidly released in response to food
A
Bolus insulin release
14
Q
Def: diabete Mellitus
A
A metabolic disorder characterized by the presence of hyperglycaemia due to defective insulin secretion, insulin action, or both.
15
Q
Type 1 Diabetes
A
Due to defective insulin secretion
An autoimmune destruction of pancreatic Beta cells causing an absolute lack of insulin secretion
16
Q
Type 2 Diabetes
A
Due to insulin resistance, eventually leading to defective insulin secretion
17
Q
Macrovascular complications of Diabetes
A
Cardiovascular disease (dyslipidemia, hypertension, coronary artery disease, stroke, erectile dysfunction)
18
Q
Microvascular complications of diabetes
A
- Nephtopathy leading to kidney impairment leading to kidney failure.
- Retinopathy potentially leading to blindness
- peripheral neuropathy leading to infection and possible amputation
19
Q
signs and symptoms of Type 1 Diabetes
A
Hyperglycemia polyuria polyphagia polydipsia glucosuria weight loss fatigue
20
Q
Diabetic ketoacidosis (DKA)
A
The body breaks down ketones for energy instead (because it can’t use glucose) leads to production of kept acids, coma, and death
21
Q
Signs and symptoms of Diabetic Ketoacidosis
A
Nausea vomiting severe abdominal pain this excessive urine production dry mouth hypotension tachycardia deep and laboured breathing (acetone) confusion ketones present in urine
22
Q
Fasting Blood Glucose level
A
“technically” no caloric intake for at least 8 hrs.
23
Q
post- prandial blood glucose level
A
taken 2 hours AFTER a meal
24
Q
Hemoglobin A1C (%)
A
Measures an average of of blood glucose over the last 3 months
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target values for A1C (adults >18)
less than or equal to 7.0% (for most)
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Taget values for Fasting glucose levels
4.0-7.0
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target values for Post Prandial Blood glucose
5. 0-10.0
| 5. 0-8.0 if A1C targets not being met
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Signs and symptoms of Hyperglycemia
```
Fasting blood glucose >7.0 mmol/L
polyuria
polydipsia
polyphagia
glucosuria
fatigue
```
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Treatment of Type 1 diabetes
Insulin - by giving insulin we try to obtain glucose homeostasis
30
MOA: Insulin detemir
Long-acting insulin analogue
- after injection the molecules self-associate and bind to albumin, and are slowly released from subcutaneous tissue into blood stream. slow predictable rate.
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MOA: Insulin glargine
Long-acting insulin analogue
- An acidic (pH of 4) product in the vial, and once injected subcutaneously, the acidic solution is neutralized and forms micro-precipitates. these slowly dissolve over at a slow predictable rate.
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what colour would a bolus insulin solution be?
Clear
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What colour would a basal insulin solution be?
cloudy - except Lantus and Levemir
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place these insulin administration site in order of fastest to slowest speed of absorption
1. arm
2. buttock
3. abdomen
4. thigh
1. abdomen
2. arm
3. thigh
4. buttock
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would absorption increase or decrease with exercise?
it would increase
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would absorption increase or decrease with cold?
it would decrease
37
how long can open vials of insulin be stored at room temperature for?
28 days
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which insulins should not be mixed with any other insulins?
Long acting insulin analogues
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When mixing 2 insulins, which should always be drawn up first?
the quick acting (bolus) insulin should always be drawn before the long acting (basal) insulin
40
what is the dawn phenomenon?
A natural increase in blood glucose that occurs 4-8am
du to in glucose production by liver and hormone sugars in morning in response to circadian rhythm - unpredictable and inconsistent
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what is the Somogyi effect?
An increase in blood glucose caused by the liver producing glucose in response to hypoglycaemia during the night.
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signs of hypoglycaemia during the night?
Nightmares
sweating
hunger
headache upon waking
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Hypoglycemia
Fasting glucose < 4 mmol/L
| LOW blood glucose. can occur if too much insulin given, improper timing of insulin, or pt skipped a meal.
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Signs and symptoms of Hypoglycemia - autonomic
```
Trembling
palpitations
sweating
anxiety
hunger
tingling
```
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Signs and symptoms of Hypoglycemia -Neuroglycopenic
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Difficulty concentrating
confusion
weakness
drowsiness
vision changes
difficulty speaking
headache
dizzeness
```
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ways to reverse hypoglycemia
15grams of simple carbohydrates
- 4, 4g glucose tablets
- 15mL water with 3tsp of sugar
- 175mL juice or regular soft drink
- 6 lifesavers
- 15mL (1 tablespoon) of honey
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Signs and symptoms of Type 2 diabetes
- MAYBE polyuria, polydipsia, nocturne, fatigue
- CAN be asymptomatic at diagnosis
- often overweight or obese
- May have already developed complications
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Classes of Oral HupOglycemics
1. Metformin
2. Sulfonylureas
3. Meglitinides
4. Thiazolidinesdiones
5. Acarbose
6. Incretins
7. SGLT-2 Inhibitors
49
MOA: Metformin
A biguanide
| enhances tissues sensitivity to insulin which reduces insulin resistance - also decreases hepatic gluconeogenesis
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Adverse effects: Metformin
nausea(take with food), diarrhea, lactic acidosis (rare)
| - does not cause hypoglycaemia on its own.
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Lactic acidosis
an accumulation of serum lactate which lowers blood pH
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signs and symptoms of lactic acidosis
```
weakness
malaise
fatigue
myalgia
heavy laboured breathing
```
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MOA: sulfonylureas
Enhances insulin secretion from the pancreas (insulin secretagogue) - also increases insulin sensitivity at target tissues (like metformin)
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Adverse effects: sulfonylureas
```
Hypoglycemia
weight gain
nausea
rash
hepatotoxicity (do NOT take with alcohol)
- avoid in elderly
- can cause hypoglycaemia on its own
```
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MOA: Meglitinides
Stimulate release of insulin from pancreas. (insulin secretagogue)
* requires presence of glucose to exert action, therefore MUST be take before (within 30min) or WITH a meal.
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Adverse effects: Meglitinides
generally only cause hypoglycaemia when combined with another hypoglycaemic drug
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MOA: Thiazolidinediones
Enhance insulin sensitivity at target tissues (similar to metformin)
food has no direct effect (can be taken with or without food)
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adverse effects: Thiazolidinediones
Edema and fluid retention, headache, weight gain
* may increase risk of fractures, some concerns about increased cardiovascular events
not likely to cause hypoglycaemia on its own
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MOA: Acarbose
Inhibits Alph-glucosidase, which blocks absorption of carbohydrates from the GI tract, preventing hyperglycaemia - must be taken WITH meals
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Adverse effects: Acarbose
Abdominal cramping
diatthea
flatulence
malabsorption of vitamins/ minerals or other drugs (separate by 2 hrs)
potential hepatoxicity
- does not cause hypoglycaemia on its own
* if hypoglycaemia DOES occur - must not take SUCROSE - only use GLUCOSE tabs, milk, or honey.
61
MOA: Inretins
* two potential aims
incretins are hormones that tell the pancreas to release insulin (from pituitary)
* 1. mimic endogenous incretin (GLP-1 agonists) OR
2. inhibit the breakdown of incretin (DPP-4 inhibitors)
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Adverse effects: Incretins
nausea
vomiting
diarrhea
edema
some concerns about pancreatitis, pancreatic cancer, and cardiovascular disease
* not likely to cause hypoglycaemia on its own
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MOA: SGLT-2 inhibitors
Increases excretion of glucose in kidney, therefor reducing blood glucose levels
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Adverse effects: SGLT-2 inhibitors
```
weight loss
diuretic effect
hypotension
polydipsia (thirst)
increased rate of UTIs
MUST have adequate kidney function*
Not likely to cause hypoglycaemia on own
```
65
Diabetes Monitoring considerations
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Blood glucose levels
Hemoglobin A1C
Signs of hypoglycaemia and hyperglycaemia
BP and pulse
Kidney function
Tingling, numbness, checking feet
Vision
Liver Enzymes
```
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stimulates the basal metabolic rate of nearly all tissues.
Thyroid gland
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Over-Abundance of thyroid hormone
Hyperthyroidism
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Inability to produce thyroid hormone
hypothyroidism
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Signs of Hyperthyroidism
Tachycardia and palpitations
hypertension
nervousness, irritability, insomnia, tremor
weight loos despite large appetite
hyperglycaemia
heat intolerance and hyperthermia, fever, sweating
eyelid lag, protruding eyes, goiter
70
Signs of hypothyroidism
```
Bradycardia
hypertension then hypotension
gradual onset of weakness and fatigue, muscle cramps
weight gain despite decreased appetite
hypoglycaemia
cold intolerance and hypothermia
dry skin and hair, delayed reflexes
```
71
What can be a cause of hypothyroidism?
Iodine deficiency. because thyroid hormone contains iodine
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classes of medications for Hypothyroidism
1. thyroid agents
A. levothyroxine (T4)
B. Other thyroid products
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classes of medications for hyperthyroidism
1. Anti-thyroid agents
A. Propylthiouracil
B. Methimazole
C. Radioactive Iodide
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MOA: Levothyroxine
Synthetically made T4 hormone which the body converts to T3 in peripheral tissues as needed.
* best absorbed on an empty stomach, 1/2 hour before eating, or 2 hours after eating.
* take in morning
75
some other thyroid products
```
Liothyronine (Synthetic T3)
Desiccated thyroid (mix of T3 and T4 obtained form dried thyroid glands from pigs)
```
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MOA: propylthioutacil (PTU)
Inhibits synthesis of thyroid hormone, as well as conversion of T4 to T3
*used short term to control thyroid function until surgery
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Adverse effects: propylthioutacil (PTU)
```
rash
symptoms of hypothyroidism
agranulocytosis
hepatotoxcitiy
many drug interactions
must be take multiple X/day
can take up to 3 wks to exert effect.
```
78
MOA: Methimazole
Inhibits synthesis of thyroid hormone, but does NOT inhibit T4 conversion.
*safe than propylthioutacil, but takes longer to work.
taken once daily
Long-term option
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MOA: radioactive Iodide
Iodine is only taken up by the thyroid. radioactivity destroys the thyroid gland. goal is to only destroy a little of it - but many result in hypothyroid state.
* can also treat thyroid cancer.
80
Monitoring: Thyroid disorders
Adverse effects r/t replacement therapies are RARE
monitoring focuses on symptoms of HYPO and HYPER thyroidism and the effectiveness of therapy
adherence and consistent administration
proper adjustment of doses.
81
What hormones are secreted by the Adrenal Glands?
Epinephrine and Norepinephrine
Mineralocorticoids - aldosterone
Glucocorticoids - Corticol
Androgens - DHEA --> testosterone
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released in response to stress (sympathetic nervous system activation)
* job is to bring body back to homeostasis
Cortisol
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Adverse effects: Corticosteroids - opthalmic
```
Stinging
redness
tearing
buring
secondary infection
*Long-term use - cataracts, glaucoma
```
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Adverse effects: Corticosteroids - Oral inhalation
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Thrush
hoarsness
dry mouth
dysphoria (change in voice)
dysphagia
taste disturbance
```
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Adverse effects: Corticosteroids - nasal inhalation
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Rhinorrhea
buring
sneezing
dry mucous membranes
epistaxis
loss of smell
```
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Adverse effects: Corticosteroids - topical
burning
irritation
skin atrophy
telangiectasia
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How to prevent adverse effects from corticosteroids ?
Lowest dose possible for shortest duration possible. apply very thin layer of product only on affected area, do NOT apply to open skin.
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```
Adverse effects: Corticosteroids with systemic administration
CNS
EYE
FACE/TRUNK
HEART
GI
BLOOD
KIDNEYS
GROWTH
MUSCLE
BONES
SKIN
```
CNS: Euphoria, insomnia, restlessness, increased appetite, altered mood,
EYE: cataracts, glaucoma
FACE/TRUNK: Redistribution of fat leading to moon face (Cushings), buffalo hump, protruding abdomen
HEART: hypertension, enlarged heart
GI: stomach upset, may increase risk of ulcer.
BLOOD: glucose intolerance leading to diabetes
KIDNEYS: fluid retention
GROTH inhibition. use cautiously in children
MUSCLE: wasting of muscle tissue
BONES: osteoporosis
SKIN: easy bruising, poor wound healing, acne, striae
89
continuous presence of cortisol (or anything that use cortisol receptor) inhibits what feedback cycle?
HPA axis - Hypothalamus Pituitary Adrenal Gland Axis
90
consequences of HPA-Axis Suppression?
If needed in a true emergency, it cannot produce cortisol to bring the body back to homeostasis
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Purpose of Pulse therapy
To induce remissions of serious conditions (MS, Lupus, Rheumatoid arthritis)
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disadvantages of pulse therapy
More likely to see hypertension, hyperglycaemia, secondary infections, and psychosis
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advantages of pulse therapy
rapid control, lower *cumulative* doses, less long-term adverse effects
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MOA: Prednisone
mimics endogenous cortisol, reducing inflammation and suppressing immune system
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indications: prednisone
For sever inflammation, exacerbation of auto-immune diseases
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adverse effects: prednisone
nausea, hypertension, hyperglycaemia, insomnia, psychosis, redistribution of fat, osteoporosis, easy bruising, infections, HPA-Axis suppression
*use short term whenever possible
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what does each Nephron consist of?
```
Glomerulus
Bowman's capsule
Proximal Tublule
Loop of hence
Distal Tubule
Collecting duct
```
98
functions of the kidney
Excretory: filtration, secretion, reabsorption, excretion
Endocrine: renin, prostaglandins, kinins, erythropoietin secretion
Metabolic: Vitamin D activation, Gluconeogenesis, Insulin metabolism
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6 functions of the kidneys
1. regulate fluid, electrolyte, and acid-base balance
2. remove metabolic waste products from blood for urinary excretion
3. removal of foreign chemicals from blood for urinary excretion
4. regulation of blood pressure
5. secretion of hormones
6. Gluconeogenesis
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Progressive loss of kidney function occurring over several month to years. characterized by gradual replacement of normal kidney architecture with fibrosis.
kidney disease
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how do we monitor kidney disease?
Serum Creatinine and calculate the creatinine clearance - and estimate of GFR
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GFR and metabolic consequences for stage 1 kidney disease
GFR Greater than or equal to 90. no obvious consequences.
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GFR and metabolic consequences for stage 2 kidney disease
GFR 60-89
| decreased calcium absorption and increased parathyroid hormone
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GFR and metabolic consequences for stage 3 kidney disease
GFR 30-59
| hypocalcemia, malnutrition, onset of anemia, onset of left ventricular hypertrophy
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GFR and metabolic consequences for stage 4 kidney disease
GFR 15-29
increased triglycerides, hyperphosphatemia, sodium/water imbalance, metabolic acidosis, tendency to hyperkalemia, hypermagnesiumia
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GFR and metabolic consequences for stage 5 kidney disease
GFR less than 15 or RRT (renal replacement therapy)
| Development of azotemia (retention of urea and nitrogenous wastes in the blood)
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interventions to delay progression of kidney disease
1. BP control
2. ACE-inhibitors /ARB therapy - indicated for Pt's with CKD in the ABSENCE of hypertension
3. Tight bloot glucose control for dabetics
4. smoking cessation
5. Avoidance of Nephrotaxins
108
medications for kidney disease
```
Diuretics (loop)
Sodium Bicarbonate
sodium polystyrene sultanate
phosphate binders, calcium, vit D
Erythropoietin and iron
Cardiovascular drugs
GI drugs
Neurologics
```
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withdrawal of progestin
causes menses
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maintenance of Progestin
Maintain a pregnancy
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Regulate uterine changes
Progestins
112
responsible for maturation of sex organs and secondary sex characteristics of female
Estrogens
113
other important metabolic effects of estrogens
```
Maintain cholesterol levels
involved with clotting factors
facilitating calcium uptake into bones
maintaining healthy vulvovaginal tissue
sexual motivation
maintaining skin collagen, elasticity and thickness
decreased gingival inflammation
```
114
MOA: Contraceptions
Delivers small doses of estrogen and progestin or progestin alone to provide negative feedback, inhibiting ovulation from occurring (preventing LH and FSH spike)
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adverse effects associated with estrogen
```
Nausea
breast tenderness
headache
bloating
thrombosis
```
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Adverse effects associated with progestins
```
irritability
fatigue
breast tenderness
bloating
withdrawal bleeding
headache
adverse lipid alterations
PMS-like symptoms
```
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MOA: mifepristone
potent progesterone receptor modulator, with strong antiprogestin and antiglucocorticoid activity
causes endometrial degeneration, uterine contractility, resumption of prostaglandin production. cerviacla softening and dilation, potential onset of bleeding
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MOA: misoprostol
potent synthetic prostaglandin, induces cervical ripening, uterine contractions, acts on GI smooth muscle.
119
Menopause
An age related decrease in number and quality of ovarian follicles - they no longer respond to FSH
- ovaries no longer produce estrogen or progestins
pituitary initially response with increased levels of FSH and LH *peri-menopause
*12 consecutive month with NO menses
120
Short term Menopausal symptoms
```
Vasomotor symptoms (photoflashes)
sleeping pattern changes (insomnia)
Mood and cognition changes
Genitourinary changes (vulvovaginal atrophy)
Sexual changes (loss of libido)
Bleeding changes (irregularity)
```
121
Long term menopausal symptoms
Osteoporosis - decline in estrogen causes increased in bone turnover and reabsorption
CVD
Hormone replacement therapy in NOT recommended solely for the purpose of preventing either osteoporosis or CVD
122
why is estrogen given with progesterone for Hormonal replacement therapies and Oral contraceptives?
Estrogen cause proliferation of the endometrial lining, it the lining does not get sloughed off the in an increased risk of endometrial cancer in postmenopausal women.
123
Selective Estrogen Receptor Modulators
Can act as both estrogen agonist and antagonist, depending upon the site of the receptor
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MOA: raloxifene
an agonist on bone and lipid receptor. preventing osteoporosis and hypercholesterolemia, but an antagonist on uterine nd great tissue
125
MOA: tamoxifen
a competitive antagonist in breast and uterine tissue which displaces endogenous estrogen (a stimulating factor for some cancers) and likely and agonist on bone endometrial and lipid receptors
126
MOA: clomiphene
Stimulates release of LH, which matures more ovarian follicles
127
MOA: human chorionic gonadotropin (HCG)
Identical to human LH, matures ovarian follicles - levels detectable inuring
128
MOA: Progestins
Presence help maintain pregnancy - can give vaginally if frequent miscarriages in early stages
129
Def: endometriosis
Presence of endometrial tissue in the locations besides the uterus. Tissue responds to Estrogens and progestins, causing severe pain, dysfunctional bleeding, and dysmenorrhea when soughing occurs
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MOA: Leuprolide
GnRH agonists that initially increase, then eventually suppress HPO-axis
131
MOA: Danazol
Pituitary gonadotropin inhibitor, suppresses HPO-axis
132
Functions of Androgens
Build muscle mass
promotes synthesis of erythropoietin
maturation of male sex organs and responsible for secondary sex characteristics of men.
133
adverse effects from anabolic steroid use: MEN
```
Raise cholesterol levels
hepatotoxicity
aggression
tumour
altered glucose tolerance
impotence
low sperm counts
```
134
adverse effects from anabolic steroid use: women
```
Raise cholesterol levels
hepatotoxicity
aggression
tumour
altered glucose
masculine appearance (irreversible deepening of voice and facial hair development)
menstrual irregularities
```
135
2 factors involved with Benign prostatic Hyperplasia
1. enlargement of prostate due to androgens (DHT)
| 2. decline in detrusor muscle strength (Alpha1 receptors) in bladder due to age
136
Benign prostatic Hyperplasia - causes
occurs when the enlarged prostate starts to push against the urethra, restricting flow of urine. the bladder wall then begins to thicken and become irritable.
137
MOA: Alpha1-Blockers
Receptos in both Smooth muscle or bladder, urethra, and prostate - relax the smooth muscle, easing urgency symptoms and possibly restriction.
*improve but do not eliminate symptoms
138
adverse effects: Alpha1-Blockers
Retrograde ejaculation
dizziness, fatigue, rhinitis
orthostatic hypotension
syncope
intraoperative floppy iris syndrom (dilates pupil)
Needs dosage adjustment for liver or kidney dysfunction
139
MOA: 5-Alpha-reductase inhibitors
Block conversion of testosterone into DHT
| CAN change prostate size.
140
adverse effects: 5-Alpha-reductase inhibitors
```
Ejaculatory dysfunction
loss of libido
impotence
gynecomastia
can cause birth defects in male children (why it is important to handle med appropriately!)
```
141
MOA: Phosphodiesterase-5 inhibitors (PDE-5-I)
Enhance nitric oxide-induces smooth muscle relaxation which allows blood flow into corpus cavernous.
must NEVER be given in addition to nitrate (potent vasodilators)
142
Adverse effects: Phosphodiesterase-5 inhibitors (PDE-5-I)
Hypotension, headache, back and muscle pain, hearing loss, visual changes, priapism (erection lasting more than 4 hours)
