Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharm 250 > Module 6 - Endocrine system > Flashcards

Module 6 - Endocrine system Flashcards

1
Q

Def: endocrine system

A

Body system which uses hormones to communicate and send messages.
regulated byt NEGATIVE feedback loops

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Some Endocrine glands

A

*Hypothalamus
*Pituitary
Thyroid and parathyroid Glands
Adrenal Glands
Pancreas
Ovaries / Testes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Exocrine function of the pancreas?

A

Secretes digestive enzymes directly into the GI tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Endocrine function of the pancreas?

A

Secretes hormones from the islets of langerhans
insulin - from Beta cells
Glucagon - from Alpha cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is Glycogen?

A

Stored Glucose.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

usual amount of Insulin secreted in a day

A

25-50 units

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

basal release rate of insulin

A

0.5-1.0 units/hour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

when would the rate of insulin release increase?

A

when blood glucose levels are >5.5mmol/L (in response to eating)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

beta cells secrete small amounts of insulin throughout the day?

A

Basal insulin release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

At meal times, insulin is rapidly released in response to food

A

Bolus insulin release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Def: diabete Mellitus

A

A metabolic disorder characterized by the presence of hyperglycaemia due to defective insulin secretion, insulin action, or both.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Type 2 Diabetes

A

Due to insulin resistance, eventually leading to defective insulin secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Macrovascular complications of Diabetes

A

Cardiovascular disease (dyslipidemia, hypertension, coronary artery disease, stroke, erectile dysfunction)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

signs and symptoms of Type 1 Diabetes

A 
Hyperglycemia 
polyuria 
polyphagia 
polydipsia 
glucosuria 
weight loss
fatigue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Fasting Blood Glucose level

A

“technically” no caloric intake for at least 8 hrs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

post- prandial blood glucose level

A

taken 2 hours AFTER a meal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Hemoglobin A1C (%)

A

Measures an average of of blood glucose over the last 3 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

target values for A1C (adults >18)

A

less than or equal to 7.0% (for most)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Taget values for Fasting glucose levels

A

4.0-7.0

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

target values for Post Prandial Blood glucose

A
  1. 0-10.0

5. 0-8.0 if A1C targets not being met

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Signs and symptoms of Hyperglycemia

A 
Fasting blood glucose >7.0 mmol/L 
polyuria 
polydipsia 
polyphagia 
glucosuria 
fatigue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Treatment of Type 1 diabetes

A

Insulin - by giving insulin we try to obtain glucose homeostasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

MOA: Insulin detemir

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

MOA: Insulin glargine

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what colour would a bolus insulin solution be?

A

Clear

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What colour would a basal insulin solution be?

A

cloudy - except Lantus and Levemir

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

place these insulin administration site in order of fastest to slowest speed of absorption

  1. arm
  2. buttock
  3. abdomen
  4. thigh
A
  1. abdomen
  2. arm
  3. thigh
  4. buttock
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

would absorption increase or decrease with exercise?

A

it would increase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

would absorption increase or decrease with cold?

A

it would decrease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

how long can open vials of insulin be stored at room temperature for?

A

28 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

which insulins should not be mixed with any other insulins?

A

Long acting insulin analogues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

When mixing 2 insulins, which should always be drawn up first?

A

the quick acting (bolus) insulin should always be drawn before the long acting (basal) insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what is the dawn phenomenon?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what is the Somogyi effect?

A

An increase in blood glucose caused by the liver producing glucose in response to hypoglycaemia during the night.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

signs of hypoglycaemia during the night?

A

Nightmares
sweating
hunger
headache upon waking

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Hypoglycemia

A

Fasting glucose < 4 mmol/L

LOW blood glucose. can occur if too much insulin given, improper timing of insulin, or pt skipped a meal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Signs and symptoms of Hypoglycemia - autonomic

A 
Trembling 
palpitations
sweating 
anxiety 
hunger 
tingling
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Signs and symptoms of Hypoglycemia -Neuroglycopenic

A 
Difficulty concentrating 
confusion 
weakness 
drowsiness 
vision changes 
difficulty speaking 
headache 
dizzeness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

ways to reverse hypoglycemia

A

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Signs and symptoms of Type 2 diabetes

A
  • MAYBE polyuria, polydipsia, nocturne, fatigue
  • CAN be asymptomatic at diagnosis
  • often overweight or obese
  • May have already developed complications
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Classes of Oral HupOglycemics

A
  1. Metformin
  2. Sulfonylureas
  3. Meglitinides
  4. Thiazolidinesdiones
  5. Acarbose
  6. Incretins
  7. SGLT-2 Inhibitors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

MOA: Metformin

A

A biguanide

enhances tissues sensitivity to insulin which reduces insulin resistance - also decreases hepatic gluconeogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Adverse effects: Metformin

A

nausea(take with food), diarrhea, lactic acidosis (rare)

- does not cause hypoglycaemia on its own.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Lactic acidosis

A

an accumulation of serum lactate which lowers blood pH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

signs and symptoms of lactic acidosis

A 
weakness 
malaise 
fatigue 
myalgia 
heavy laboured breathing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

MOA: sulfonylureas

A

Enhances insulin secretion from the pancreas (insulin secretagogue) - also increases insulin sensitivity at target tissues (like metformin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Adverse effects: sulfonylureas

A 
Hypoglycemia
weight gain 
nausea 
rash 
hepatotoxicity (do NOT take with alcohol)
- avoid in elderly 
- can cause hypoglycaemia on its own
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

MOA: Meglitinides

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Adverse effects: Meglitinides

A

generally only cause hypoglycaemia when combined with another hypoglycaemic drug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

MOA: Thiazolidinediones

A

Enhance insulin sensitivity at target tissues (similar to metformin)
food has no direct effect (can be taken with or without food)

58
Q

adverse effects: Thiazolidinediones

A

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
59
Q

MOA: Acarbose

A

Inhibits Alph-glucosidase, which blocks absorption of carbohydrates from the GI tract, preventing hyperglycaemia - must be taken WITH meals

60
Q

Adverse effects: Acarbose

A

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
Q

MOA: Inretins

  • two potential aims
A

incretins are hormones that tell the pancreas to release insulin (from pituitary)

    1. mimic endogenous incretin (GLP-1 agonists) OR
      1. inhibit the breakdown of incretin (DPP-4 inhibitors)
62
Q

Adverse effects: Incretins

A

nausea
vomiting
diarrhea
edema
some concerns about pancreatitis, pancreatic cancer, and cardiovascular disease
* not likely to cause hypoglycaemia on its own

63
Q

MOA: SGLT-2 inhibitors

A

Increases excretion of glucose in kidney, therefor reducing blood glucose levels

64
Q

Adverse effects: SGLT-2 inhibitors

A 
weight loss
diuretic effect 
hypotension 
polydipsia (thirst)
increased rate of UTIs 
MUST have adequate kidney function* 
Not likely to cause hypoglycaemia on own
65
Q

Diabetes Monitoring considerations

A 
Blood glucose levels 
Hemoglobin A1C
Signs of hypoglycaemia and hyperglycaemia 
BP and pulse 
Kidney function 
Tingling, numbness, checking feet 
Vision 
Liver Enzymes
66
Q

stimulates the basal metabolic rate of nearly all tissues.

A

Thyroid gland

67
Q

Over-Abundance of thyroid hormone

A

Hyperthyroidism

68
Q

Inability to produce thyroid hormone

A

hypothyroidism

69
Q

Signs of Hyperthyroidism

A

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
Q

Signs of hypothyroidism

A 
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
Q

What can be a cause of hypothyroidism?

A

Iodine deficiency. because thyroid hormone contains iodine

72
Q

classes of medications for Hypothyroidism

A
  1. thyroid agents
    A. levothyroxine (T4)
    B. Other thyroid products
73
Q

classes of medications for hyperthyroidism

A
  1. Anti-thyroid agents
    A. Propylthiouracil
    B. Methimazole
    C. Radioactive Iodide
74
Q

MOA: Levothyroxine

A

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
Q

some other thyroid products

A 
Liothyronine (Synthetic T3)
Desiccated thyroid (mix of T3 and T4 obtained form dried thyroid glands from pigs)
76
Q

MOA: propylthioutacil (PTU)

A

Inhibits synthesis of thyroid hormone, as well as conversion of T4 to T3
*used short term to control thyroid function until surgery

77
Q

Adverse effects: propylthioutacil (PTU)

A 
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
Q

MOA: Methimazole

A

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

79
Q

MOA: radioactive Iodide

A

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
Q

Monitoring: Thyroid disorders

A

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
Q

What hormones are secreted by the Adrenal Glands?

A

Epinephrine and Norepinephrine
Mineralocorticoids - aldosterone
Glucocorticoids - Corticol
Androgens - DHEA –> testosterone

82
Q

released in response to stress (sympathetic nervous system activation)
* job is to bring body back to homeostasis

A

Cortisol

83
Q

Adverse effects: Corticosteroids - opthalmic

A 
Stinging 
redness 
tearing 
buring 
secondary infection 
*Long-term use - cataracts, glaucoma
84
Q

Adverse effects: Corticosteroids - Oral inhalation

A 
Thrush
hoarsness 
dry mouth 
dysphoria (change in voice) 
dysphagia 
taste disturbance
85
Q

Adverse effects: Corticosteroids - nasal inhalation

A 
Rhinorrhea
buring 
sneezing 
dry mucous membranes 
epistaxis 
loss of smell
86
Q

Adverse effects: Corticosteroids - topical

A

burning
irritation
skin atrophy
telangiectasia

87
Q

How to prevent adverse effects from corticosteroids ?

A

Lowest dose possible for shortest duration possible. apply very thin layer of product only on affected area, do NOT apply to open skin.

88
Q 
Adverse effects: Corticosteroids with systemic administration
CNS
EYE
FACE/TRUNK
HEART
GI
BLOOD
KIDNEYS 
GROWTH
MUSCLE 
BONES
SKIN
A

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
Q

continuous presence of cortisol (or anything that use cortisol receptor) inhibits what feedback cycle?

A

HPA axis - Hypothalamus Pituitary Adrenal Gland Axis

90
Q

consequences of HPA-Axis Suppression?

A

If needed in a true emergency, it cannot produce cortisol to bring the body back to homeostasis

91
Q

Purpose of Pulse therapy

A

To induce remissions of serious conditions (MS, Lupus, Rheumatoid arthritis)

92
Q

disadvantages of pulse therapy

A

More likely to see hypertension, hyperglycaemia, secondary infections, and psychosis

93
Q

advantages of pulse therapy

A

rapid control, lower cumulative doses, less long-term adverse effects

94
Q

MOA: Prednisone

A

mimics endogenous cortisol, reducing inflammation and suppressing immune system

95
Q

indications: prednisone

A

For sever inflammation, exacerbation of auto-immune diseases

96
Q

adverse effects: prednisone

A

nausea, hypertension, hyperglycaemia, insomnia, psychosis, redistribution of fat, osteoporosis, easy bruising, infections, HPA-Axis suppression
*use short term whenever possible

97
Q

what does each Nephron consist of?

A 
Glomerulus 
Bowman's capsule 
Proximal Tublule 
Loop of hence 
Distal Tubule 
Collecting duct
98
Q

functions of the kidney

A

Excretory: filtration, secretion, reabsorption, excretion
Endocrine: renin, prostaglandins, kinins, erythropoietin secretion
Metabolic: Vitamin D activation, Gluconeogenesis, Insulin metabolism

99
Q

6 functions of the kidneys

A
  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
100
Q

Progressive loss of kidney function occurring over several month to years. characterized by gradual replacement of normal kidney architecture with fibrosis.

A

kidney disease

101
Q

how do we monitor kidney disease?

A

Serum Creatinine and calculate the creatinine clearance - and estimate of GFR

102
Q

GFR and metabolic consequences for stage 1 kidney disease

A

GFR Greater than or equal to 90. no obvious consequences.

103
Q

GFR and metabolic consequences for stage 2 kidney disease

A

GFR 60-89

decreased calcium absorption and increased parathyroid hormone

104
Q

GFR and metabolic consequences for stage 3 kidney disease

A

GFR 30-59

hypocalcemia, malnutrition, onset of anemia, onset of left ventricular hypertrophy

105
Q

GFR and metabolic consequences for stage 4 kidney disease

A

GFR 15-29
increased triglycerides, hyperphosphatemia, sodium/water imbalance, metabolic acidosis, tendency to hyperkalemia, hypermagnesiumia

106
Q

GFR and metabolic consequences for stage 5 kidney disease

A

GFR less than 15 or RRT (renal replacement therapy)

Development of azotemia (retention of urea and nitrogenous wastes in the blood)

107
Q

interventions to delay progression of kidney disease

A
  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
Q

medications for kidney disease

A 
Diuretics (loop) 
Sodium Bicarbonate 
sodium polystyrene sultanate 
phosphate binders, calcium, vit D
Erythropoietin and iron 
Cardiovascular drugs 
GI drugs 
Neurologics
109
Q

withdrawal of progestin

A

causes menses

110
Q

maintenance of Progestin

A

Maintain a pregnancy

111
Q

Regulate uterine changes

A

Progestins

112
Q

responsible for maturation of sex organs and secondary sex characteristics of female

A

Estrogens

113
Q

other important metabolic effects of estrogens

A 
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
Q

MOA: Contraceptions

A

Delivers small doses of estrogen and progestin or progestin alone to provide negative feedback, inhibiting ovulation from occurring (preventing LH and FSH spike)

115
Q

adverse effects associated with estrogen

A 
Nausea 
breast tenderness 
headache 
bloating
thrombosis
116
Q

Adverse effects associated with progestins

A 
irritability 
fatigue 
breast tenderness
bloating 
withdrawal bleeding 
headache 
adverse lipid alterations 
PMS-like symptoms
117
Q

MOA: mifepristone

A

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

118
Q

MOA: misoprostol

A

potent synthetic prostaglandin, induces cervical ripening, uterine contractions, acts on GI smooth muscle.

119
Q

Menopause

A

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
Q

Short term Menopausal symptoms

A 
Vasomotor symptoms (photoflashes)
sleeping pattern changes (insomnia)
Mood and cognition changes 
Genitourinary changes (vulvovaginal atrophy) 
Sexual changes (loss of libido) 
Bleeding changes (irregularity)
121
Q

Long term menopausal symptoms

A

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
Q

why is estrogen given with progesterone for Hormonal replacement therapies and Oral contraceptives?

A

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
Q

Selective Estrogen Receptor Modulators

A

Can act as both estrogen agonist and antagonist, depending upon the site of the receptor

124
Q

MOA: raloxifene

A

an agonist on bone and lipid receptor. preventing osteoporosis and hypercholesterolemia, but an antagonist on uterine nd great tissue

125
Q

MOA: tamoxifen

A

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
Q

MOA: clomiphene

A

Stimulates release of LH, which matures more ovarian follicles

127
Q

MOA: human chorionic gonadotropin (HCG)

A

Identical to human LH, matures ovarian follicles - levels detectable inuring

128
Q

MOA: Progestins

A

Presence help maintain pregnancy - can give vaginally if frequent miscarriages in early stages

129
Q

Def: endometriosis

A

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

130
Q

MOA: Leuprolide

A

GnRH agonists that initially increase, then eventually suppress HPO-axis

131
Q

MOA: Danazol

A

Pituitary gonadotropin inhibitor, suppresses HPO-axis

132
Q

Functions of Androgens

A

Build muscle mass
promotes synthesis of erythropoietin
maturation of male sex organs and responsible for secondary sex characteristics of men.

133
Q

adverse effects from anabolic steroid use: MEN

A 
Raise cholesterol levels 
hepatotoxicity 
aggression 
tumour 
altered glucose tolerance 
impotence 
low sperm counts
134
Q

adverse effects from anabolic steroid use: women

A 
Raise cholesterol levels 
hepatotoxicity 
aggression 
tumour 
altered glucose 
masculine appearance (irreversible deepening of voice and facial hair development) 
menstrual irregularities
135
Q

2 factors involved with Benign prostatic Hyperplasia

A
  1. enlargement of prostate due to androgens (DHT)

2. decline in detrusor muscle strength (Alpha1 receptors) in bladder due to age

136
Q

Benign prostatic Hyperplasia - causes

A

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
Q

MOA: Alpha1-Blockers

A

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
Q

adverse effects: Alpha1-Blockers

A

Retrograde ejaculation
dizziness, fatigue, rhinitis
orthostatic hypotension
syncope
intraoperative floppy iris syndrom (dilates pupil)
Needs dosage adjustment for liver or kidney dysfunction

139
Q

MOA: 5-Alpha-reductase inhibitors

A

Block conversion of testosterone into DHT

CAN change prostate size.

140
Q

adverse effects: 5-Alpha-reductase inhibitors

A 
Ejaculatory dysfunction 
loss of libido 
impotence 
gynecomastia 
can cause birth defects in male children (why it is important to handle med appropriately!)
141
Q

MOA: Phosphodiesterase-5 inhibitors (PDE-5-I)

A

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
Q

Adverse effects: Phosphodiesterase-5 inhibitors (PDE-5-I)

A

Hypotension, headache, back and muscle pain, hearing loss, visual changes, priapism (erection lasting more than 4 hours)

Pharm 250 (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions