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PAS 506 > Exam 6 (Renal and GU) > Flashcards

Exam 6 (Renal and GU) Flashcards

1
Q

Where is right kidney

A

Under liver.
L1-L4

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2
Q

Where is left kidney

A

T12-L3

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3
Q

Hilum

A

Central region where ureter, renal artery, and renal vein attach to kidneys

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4
Q

Ureter

A

Connects kidney to bladder constantly draining urine into bladder.
Exits kidney at ureteropelvic junction

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5
Q

Kidney cortex

A

Outer region.
URINARY GENERATION
Holds renal capsule, PCT, DCT, glomeruli

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6
Q

Kidney Medulla

A

Middle layer
URINARY GENERATION AND DRAINAGE
Consists of medullary pyramids, renal columns, loop. of henle, collecting ducts

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7
Q

Pelvis of Kidney

A

Inner central cavity
URINARY DRAINAGE
Empties into ureter

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8
Q

Blood flow through kidney

A

Bowman’s capsule –> Proximal tubule -> Descending loop of Henle –> Ascending loop of Henle –> Distal tubule

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9
Q

Nephron

A

Functional unit of kidney
Millions in each kidney.
Mostly in cortex
Bowman’s capsule
PCT
Loop of Henle
DCT
Collecting duct

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10
Q

Cortical Nephrons

A

85% of nephrons
In outer cortex
Loop of Henle short
Filter toxins and regulate Electrolytes
Less strict in filtration

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11
Q

Juxtamendullary Nephrons

A

15% of nephrons
Deep in cortex
Loop of Henle long so project into medulla
Reabsorb higher higher proprtion of glomerular FILTRATION rate.
Stimulate Na retention in states of low perfusion

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12
Q

Glomerulus

A

Filter
Primary site of urine formation
In Bowman’s Capsule

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13
Q

Bowman’s Capsule

A

Double walled funnel
Reservoirs for glomerular filtrate

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14
Q

PCT

A

Proximal convoluted tubule
High water permeability
2/3 glomelular filtrate reabsorbed
Reabsorbs NaHCO3, NaCL, K, glucose, AA, water
Adjusts pH

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15
Q

Loop of Henle

A

Allows water to pass from filtrate to interstitial fluid.
Ascending limb is water impermeable.
Descending limb is water permeable

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16
Q

Distal tubule

A

Selectively secretes and absorbs ions to maintain blood pH and electrolytes

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17
Q

Collecting ducts

A

Rabsorbs solutes and water from filtrate

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18
Q

Glomerular filtration barrier layers

A
  1. Fenestrated endothelium
  2. Glomerular basement membrane
  3. Podocyte slit diaphragm
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19
Q

Podocytes

A

Form slit diaphragm of glomerullus

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20
Q

Steps of Urine formation

A
  1. Glomerular Filtration
  2. Tubular reabsorption
  3. Tubular secretion
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21
Q

Why does the kidney excrete electrolytes

A

AWETBED
Acid-base balance
Water balance
Electrolyte balance
Removal of toxins
BP control
Erythropoietin production
D vitamin metabolism

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22
Q

ADH effect on kidney

A

Permeability of collecting tubules
Fluid regulation
Increases water reabsorption
Affects specific gravity

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23
Q

Aldosterone

A

Increases water and Na absorption by DCT.
Decreases potassium by increasing excretion.
Made and released by adrenal cortex

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24
Q

Calcitriol

A

Converted from calcidiol into calcitriol (active form of vitamin D) by kidney

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25
Q

Erythropoietin

A

Stimulates red blood cell production in bone marrow.
Released from kidneys when O2 is low.

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26
Q

Renalase

A

Metabolizes catecholamines, affects HR and BP

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27
Q

Renin

A

BP regulation via angiotensin
Released from kidneys when BP low to start RAAS pathway

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28
Q

Kidney role in glucose regulation

A

Catabolism of peptide hormones like insulin.
Can perform gluconeogenesis during times of fasting

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29
Q

How much cardiac output goes to kidneys

A

20-25%

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30
Q

Decreased perfusion to kidney

A

Stimulates RAAS system to increases blood pressure

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31
Q

Prerenal failure

A

Most common
Caused by decreased perfusion

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32
Q

Intrarenal failure

A

Direct damage to renal parnchyma

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33
Q

Postrenal failure

A

Obstruction

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34
Q

Types of acute renal failure

A

Prerenal
Intrarenal
Postrenal

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35
Q

Chronic Renal failure

A

Lasts longer than 3 months

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36
Q

Three phases of acute kidney injury

A

Oliguric - decreased output
Diuretic - increased output
Recovery - GFR normalizes

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37
Q

First phase of acute kidney injury

A

Oliguric
Decreased urine output
Edema
Decreased Na and water absorption
Hypervolemic
Weight gain
HTN
BUN and creatinine levels rise

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38
Q

Second phase of acute kidney disease

A

Diuretic
Increased urine output
Improved Na and water absorption.
Hypokalemia and hyponatremia can occur.
Hypovolemic
Weight loss
Dehydration
BUN and creatinin levels rise

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39
Q

Third phase of kidney disease

A

Recovery
Normal urine output
Recovery of GFR

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40
Q

Renal failure symptoms

A

Hyper/hypotension depending on phase
Dy mucous membrane
Poor skin turgor
Decrease/increase urine output depending on phase.
Mental status changes
Muscle aches
Nausea

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41
Q

First thing to look at to check for renal failure

A

Look at urine output and concentration of the urine (color)

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42
Q

First sign of kidney failure in lab

A

Albumin in the urine

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43
Q

First sign of kidney failure

A

Decreased urine output

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44
Q

Most accurate measure of GFR

A

Creatinine clearance because creatinine is filtered by glomeruli but not reabsorbed by tubules

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45
Q

Cast formation

A

Occurs in DCT and collecting ducts when Tamm-Horsfall protein is secreted by epithelial tube cells.

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46
Q

Tam Horsfall protein

A

Attracts adhesion of other tubular particles (cells, bile, hemoglobin, albumin, immunoglobulins).
Forms casts

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47
Q

Five main sections of nephrons

A

Glomerulus
PCT
Thin descending and thick ascending loop of Henle
DCT
Collecting duct

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48
Q

Diuretics that work in PCT

A

Carbonic anhydrase inhibitors
Osmotic diuretics

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49
Q

Diuretics that work in loop of henle

A

Loop diuretics

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50
Q

Diuretics that work in DCT

A

Thiazides

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51
Q

Diuretics that work in collecting duct

A

Potassium sparing diuretics
(Aldosterone inhibitors
Epithelial sodium channel antagonists)

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52
Q

What regulates bicarbonate reabsorption in PCT

A

Carbonic anhydrase

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53
Q

PCT drug targets

A

Carbonic anhidrase
SGLT2
Osmolality (Mannitol)

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54
Q

Thick ascending limb of Loop of Henle

A

High in NaCl reabsorption via Na/K/Cl cotransporter (NKCC2).
Diluted in lumen.
Impermeable
K transported through NKCC2

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55
Q

Loop of Henle drug target

A

N/K/CL cotransporter type 2 (NKCC2)

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56
Q

DCT

A

Distal convoluted tubule
NaCl reabsorption via Na/Cl cotransporter (NCC)
Dilutes tubular fluid
Results impermeability to water

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57
Q

DCT drug target

A

Na/Cl cotransporter
Thiazide diuretics

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58
Q

Collecting duct system

A

Final site of NaCl reabsorption
Determines Na concentration
Most important site of K secretion

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59
Q

Principal cells

A

In Collecting duct
Na reabsorption
K excretion
Water transport
No apical cotransporters
Regulated by aldosterone

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60
Q

Intercalated cells

A

In collecting duct.
Alpha does H secretion
Beta does bicarbonate secretion

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61
Q

Na and K relationship

A

Na transported back to blood via Na/K pump.
Na reabsorption happens more often than K secretion resulting in negative lumen.
Drives Cl back into blood.
Draws K into lumen from cell

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62
Q

Principal cells drug targets

A

Potassium sparing diuretics
Aldosterone receptor for potassium aldosterone antagonists
Epithelial Na channel for and epithelial Na channel antagonists

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63
Q

Acetazolamide

A

Carbonic anhydrase inhibitor
Decreases NaHCO3 rabsorpton
Attack at PCT

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64
Q

Carbonic anhydrase inhibitor mechanism

A

Acetazolamide
Blocks carbonic anhydrase thus inhbiting formation of carbonic acid.
Carbonic acid doesn’t dissociate into HCO3 and H.
No driving force for Na to be reabsorbed
Increased Na excretion in PCT

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65
Q

Acetazolamide uses

A

Carbonic anhydrase inhibitor
NOT used as diuretic
Glaucoma
Urinary alkalinization
Metabolic alkalosis
Acute altitude sickness

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66
Q

Acetazolamide adverse effects

A

Drowziness
Metabolic acidosis
Renal stones
K wasting
Neurotoxicity if renal failure

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67
Q

Mannitol

A

Osmotic diuretic
Solute that draws water out of cells.
Decreases intracranial pressure
Not really used as diuretic

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68
Q

Loop diuretics

A

Most effective (potent) diuretic against highest reabsorption of NaCl in thick ascending limb of Henle’s loop

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69
Q

Loop diuretics mechanism

A

Inhibits NKCC2 in thick ascending limb.
Decreases reabsorption of Na K Cl
Diminish lumen positive potential increasing secretion of K Mg and Ca.

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70
Q

Loop diuretics uses

A

Acute pulmonary edema.
Hyperkalemia
Hypercalcemia

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71
Q

Loop diuretic adverse effects

A

Acute hypovalemia (hypotension)
Hypokalemia
Hypomagnesemia
Ototoxicity
Hyperuricemia

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72
Q

Thiazides mechanism

A

Block Na Cl cotransporter in DCT decreasing Na and Cl reabsorption.
Low ceiling - at certain dose we don’t see increased effect

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73
Q

Thiazide uses

A

HTN
Heart failure
Prevention of Ca containing kidney stones caused by hypercalciuria

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74
Q

Thiazide adverse effects

A

Hypercalcemia
Hyperuricemia
Hyperglycemia
Hyperlipidemia
Hypokalemia
Hypomagnesemia
Hyponatremia
Hypovolemia

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75
Q

Potassium sparing diuretics

A

Antagonize effects of aldosterone by inhibiting Na reabsorption and inhibiting K excretion.
Aldosterone antagonists
Epithelial Na channel antagonists

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76
Q

Aldosterone antagonists method of action

A

Potassium sparing
Inhibit aldosterone receptor.
Decreases reabsorption of Na.
Decreases secretion of K

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77
Q

Spironolactone

A

Aldosterone antagonist
Potent inhibitor of aldosterone receptor
Used in acne and hirsutism.
Active at progesterone receptors

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78
Q

Eplerenone

A

Aldosterone antagonist
Less active on androgen and progesterone receptors

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79
Q

ENaC Antagonist mechanism

A

Potassium sparing diuretic.
Directly inhibits ENaC leading to decrease of Na reabsorption and decrease of K secretion.

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80
Q

ENaC antagonist

A

Potassium sparing diuretic
Mostly ued for K sparing effects, not diuretic effects
Ex. amiloride triametrene

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81
Q

Amiloride

A

ENaC that is not metabolized

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82
Q

Triametrene

A

ENaC that is metabolized.
Has very short half life

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83
Q

Potassium sparing diuretic uses

A

Edema
Hypokalemia
Heart failure
Resistant hypertension
Polycystic ovary syndrome

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84
Q

Potassium sparing diuretics adverse effects

A

Hyperkalemia
Spironolactone-gynecomastia
Triamterene (kidney stones)

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85
Q

Wolffian ducts

A

Become male reproductive organs
AKA mesonephric

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86
Q

Mullerian ducts

A

What become female reproductive organs

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87
Q

Reproductive embriology order in males

A

Primordial germ cells–> Spermatagonia + Sertoli cells–> Male gametes

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88
Q

Leydig cells

A

Produce testosterone

89
Q

What causes differentiation in whether something ends up male or female

A

Presence of testosterone.
Decided at fertilization though
XY vs XX

90
Q

Primordial germ cells

A

What males and females both start out as

91
Q

Reproductive embryology order in females

A

Primordial germ cells –> oogonia –> granulosa and thecal cells –> estrogen and progestin in mature females
NO testosterone during this point so Wolffian duct degenerates

92
Q

Complete Androgen Insensitivity Syndrome

A

46 XY DSD
Genotypically male but phenotypically female
No androgen receptors so testosterone can’t do its job.
Diagnosed by failure of menstrual cycle

93
Q

Deficiency of 5 alpha-reductase

A

46 XY DSD
Genotypically male but phenotypically female
No 5 alpha reductase to convert testosterone into DHT (usable form)

94
Q

Congenital Adrenal Hyperplasia

A

46 XX DSD
Genotypically female but phenotypically male
Impaired cortisol synthesis.
Virilization of female fetus
Excessive/deficient production of androgens/hormones

95
Q

When do testes begin to enlarge

A

9-14

96
Q

Male puberty

A

Testes inlarge
Spermatogenesis in seminiferous tubules
Scrotum and penis enlarge
INcreased testosterone leads to thicker hair, deeper voise, increased muscle strength

97
Q

When does breast enlargement start

A

8-10

98
Q

Female puberty

A

Breast enlargement
Ovarian cycle starts
ENlargement of uterus, labia majora, and labia minora
Widening of pelvis

99
Q

Menarche

A

First period

100
Q

Adrenarche

A

Surge of hormones and androgens leading to pubic and axillary hair before puberty

101
Q

Precocious puberty

A

Early puberty

102
Q

Gynecomastia

A

Enlargement of male breast
Occurs when estrogen levels are elevated in neonatal period or before normal male puberty.
Also can happen in elderly men

103
Q

Testicle function

A

Secreting testosterone and make sperm

104
Q

Epidymitis function

A

Store sperm

105
Q

Vas deferens function

A

Expel sperm to urethra during ejaculation

106
Q

Semeinal vesicles function

A

Produce fluid for nourishment for ejaculated sperm

107
Q

Prostate gland function

A

Secretes acid phosphatase, contracts to deliver secretions into urethra, and liquifies semen until it gets to female reproductive tract.
Makes prostate specific antigen

108
Q

Penis function

A

Urination and intercourse

109
Q

Three phases of spermatogenesis

A
  1. Proliferation of spermatogonia
    2.Generation of genetic diversity via miosis
  2. Maturation of sperm
110
Q

LH job in males

A

Stimulate Leydig cells to PRODUCE testosterone

111
Q

FSH job in males

A

Stimulates Sertoli cells to secrete androgen binding protein that INCREASES testosterone.
Inhibin also secreted from sertoli cells that works in negative feedback against FSH

112
Q

Phases of ejaculation

A
  1. Erection
  2. Emission
  3. Ejaculation
113
Q

Erection

A

Sinusoidal spaces fill with blood

114
Q

Emission

A

Spermatozoa and seminal plasma move into urethra

115
Q

Ejaculation

A

Semen ejected from urethra

116
Q

Stages of sexual response

A
  1. Excitement
  2. Plateau
  3. Orgasm
  4. Resolution
117
Q

Excitement phase of sex

A

Penile erection
Vaginal lubrication

118
Q

Plateau phase of sex

A

Vascular congestion
Engorgement of scrotum and labia

119
Q

Orgasm phase of sex

A

Ejaculation in males
Pleasure
Rhythmic contractions of perineum

120
Q

Resolution phase of sex

A

Penile falccidity
Vaginal relaxation
Refractory period in males

121
Q

Ovaries

A

Where oogenesis occurs and eggs formed
Major source of sex steroids and hormones

122
Q

Fallopian tubes

A

Transport ovum and sperm to fertillization
Transports zygote to uterus for implantatoin

123
Q

Where does fertilization happen

A

Ampulla of Fallopian tube

124
Q

Uterus

A

Supports growing fetus during preg.
Undergoes dramatic changes during menstrual cycle.
Growth through hyperplasia in preg.
Fundus
Corpus
Cervix

125
Q

Vagina

A

Receive penis in intercourse
Temporarily retain sperm
Tube extending from cervix to vaginal opening.
Many mucus secreting glands for lubrication

126
Q

Pelvic inflammatory disease

A

Caused by STD.
Usually chlamydia and gonorrhea

127
Q

What increases risk of ectopic pregnancy

A

SCarred fallopian tubes.
Most common site of implantation in ectopic preg is ampulla

128
Q

Fundus

A

In Uterus.
Area above opening to fallopian tubes

129
Q

Corpus

A

Main body of uterus

130
Q

Cervix

A

lower portion of uerus that extends and protrudes into vagina

131
Q

Vulva

A

Collective name for female external genitalia Includes Lower 1/3 of vagina, labia, clitorus

132
Q

Where does Oogenesis occur

A

Ovaries

133
Q

Oogenesis

A

Forming of eggs
OOgonium –> 1º Oocyte –> 2º Oocyte –> Ovum

134
Q

Graafian Follicle

A

Dominant Follicle
Emerges and LH surge makes it a secondary Oocyte.
Bursts and ruptures during period

135
Q

When is Oogenesis complete

A

Fertilization
Becomes Ovum

136
Q

Menstrual cycle phases

A
  1. Follicular- 1-14
  2. Ovulatory - 13-15
  3. Luteal - 15-28
137
Q

Follicular phase

A

Days 1-14
Day 1 is first day of bleeding
Primary follicles develop
Dominant follicle emerges

138
Q

Ovulatory phase

A

Days 13-15
LH surge and increased estrogen
Ptimary oocyte completed meiosis I
Dominant follicle rupture causing ovulation.
Oocyte released

139
Q

Best time to get pregnant

A

Days 12-14

140
Q

When is ovulaton

A

Day 14

141
Q

Luteal Phase

A

Days 15-28
Corpus luteum formed
If no preg corpus luteum degenerates.
If preg continued progesterone secretion essential.

142
Q

Hydatidiform mole

A

Benign molar pregnancy
Incompatible with life.
Looks like cluster of grapes

143
Q

Implantation

A

Fertilized egg develops 6-7 days prior to implantation.
Now a blastocyst
Endometrium develops

144
Q

3 stages of implantation

A

1.Apposition - formation of loose connection in endometrium
2.Adhesion - microvilli extend from cell
3. Invasion - Embryo becomes completely embedded in endometrium of uterus

145
Q

Placenta function

A

Transport glucose, LDL, AA, large molecules to fetus between maternal and fetal circulations.
Secretion of hormones to maintain function

146
Q

Placenta hormone secretion

A

Estrogen for growth of uterus starts 12 weeks in.
Progesterone starts at 9 weeks in
Progesterones for maintaining endometrium and reducing uterine contractions to prevent premature birth.
Progesterone drops at the end of preg to let birth happen
Estrogen drops at end to allow milk let down

147
Q

Placental peptides examples

A

Human chorionic gonadotropin (hCG)
Human chorionic somatomammotropin hormone (hCS)
Start off high at begining of preg. Drop off at the end

148
Q

hCG

A

Human chorionic gonadotropin
Placental peptides
Keeps corpus luteum from degenerating.
Allows ocntinued progesterone to be secreted for early preganncy until placenta can take over making and secreting progesterone

149
Q

hCS

A

Human chorionic somatomammotropin hormone
Plancental hormone
Stimulates production of fatty acid and ketones for energy for fetus and placenta
Promotes mammary gland development
Creates state of insulin resistance in mother to promote availability of glucose for fetus

150
Q

What keeps labor going (parturition)

A

Prostaglandin and oxytocin

151
Q

Phase 0 of parturition uterine activity

A

Majority of pregnancy with uterus inactive/relaxed

152
Q

Phase 1 of parturition uterine activity

A

Cervix dilates and amniotic fluid ruptures (water breaks).
False contractions

153
Q

Phase 2 of parturition uterine activity

A

Fetus is expelled from uterus

154
Q

Phase 3 of parturition uterine activity

A

Placenta is birthed

155
Q

What is breast milk made of

A

Lactose
Triglycerides
Protein

156
Q

Colostrum

A

Liquid gold.
Very nutritious breast milk made after first few days of parturition

157
Q

What hormone does breast milk production

A

Prolactin

158
Q

What stimulates milk let down

A

Oxytocin. Works in positive feedback loop.

159
Q

When does milk production start

A

about 2 days after parturition because estrogen and progesterone were just very high

160
Q

Suckling reflexes

A

Prolactin and oxytocin stimulated by baby sucking on breast. Positive feedback

161
Q

What happens to other organ systems during preg

A

Blood volume and coagulabibity increases\
Alveolar ventilation increases
GFR increases
Nutritional demands increase
Suppression of immunity

162
Q

Overactive bladder meds

A

Antimuscarinics
beta-3 adrenergic agonists (-begron)

163
Q

Benign prostatic hyperplazsia drugs

A

alpha-1 adrenergic agonist (-osin)
5-alpha reductase inhibitors (-asteride)

164
Q

Overactive bladder

A

Frequent strong urge to urinate even when not really necessary

165
Q

Goals of overactiv bladder meds

A

Decrease urge frequency
Increase voided volume

166
Q

Antimuscarinic meds mechanism

A

Block M3 receptors on bladder.
Decreases freq of bladder contractions and increases capacity

167
Q

Most selective antimuscarinics

A

DariFENACIN
SoliFENACIN
Fewer adverse effects

168
Q

Trospium

A

Antimuscarinic
Doesn’t undergo CYP450 metabolism.
So good option for someone in liver failure
Does not cross BBB so fewer CNS effects

169
Q

Antimuscarinic adverse effects

A

Dry mouth
Constipation
Blurred vision
CNS impairments

170
Q

Ocybutyynin

A

Antimuscarinic
OTC patch
Gel

171
Q

Beta-3 adrenergic agonist mechanism

A

Bind and activate B3 adrenergic receptors.
Increases cAMP
Relaxes detrusor muscle increasing bladder capacity

172
Q

Beta-3 adrenergic agonist adverse effects

A

Urinary retention
UTI
Mirabegron increases BP inhibits CYP2D6, and causes angiodema

173
Q

Benign prostatic hyperplasia (BPH)

A

Non-malignant enlargement of prostate
Common in men over 60
Increase in size (static) and/or tone (dynamic)

174
Q

alpha-1 adrenergic antagonist

A

-osin
address tone of prostate

175
Q

alpha-1 adrenergic receptors subtypes locations

A

A - prostate
B - prostate and vasculature
D - vasculature

176
Q

alpha-1 adrenergic antagonist mechanism

A

Block prostatic alpha-1A and alpha1-B this is in prostate and blood vessels

177
Q

Adrenergic antagonis selective for alpha 1A

A

Silodosin
Tamsulosin
no Z in name

178
Q

alpha-1 adrenergic receptor antagonist adverse effects

A

Dizziness
Orthostatic hypotension
Tachycardia
Drowsiness
Inhibition of ejaculation
Retrograde ejaculation (shooting blanks)

179
Q

5-alpha reductase inhibitors

A

-asteride (five asteroids coming to blow up prostate to reduce size)
Address size of prostate

180
Q

5-alpha reductase inhibitor mechanism

A

Irriversibly inhibits alpha-5 reductase.
Testosterone not turned into usable form DHT.
Decreased growth signaling
Improved urine flow

181
Q

5-alpha reductase inhibitor Adverse Effects

A

Risk of prostate cancer.
Decreased ejaculate and libido
Erectile disfunction
Oligospermia
Teratogenic

182
Q

Day 2-7

A

FSH increase

183
Q

Day 7

A

Estrogen increase

184
Q

Day 14

A

LH FSH surge in response to estrogen causing ovulation

185
Q

Day 15

A

Ovulation.
Progesterone increases

186
Q

Day 21-28

A

Estrogen and progesterone drop if no fertilization

187
Q

Day 28

A

Wthdrawal of estrogen and progesterone

188
Q

Estrogen use as contraceptive

A

Blocks GnRH production from hypothalamus and FSH production from ant pit.
Prevents follicle development

189
Q

Progestin use as contraceptive

A

Blocks GnRH production from hypothalamus and LH production from ant pit.
No LH surge preventing ovulation half the time
Thickens cervical mucus to inhibit sperm migration.
Thins endometrium

190
Q

What are the type of hormonal contraceptive

A

Estrogen and progestin
Or just progestin

191
Q

Most common estrogen component in oral contraceptiv

A

Ethinyl estradiol

192
Q

What is the design of taking birth control pills

A

21 active tablets
7 placebo tablets
mimic the natural process

193
Q

Is combined pill or progestin only pill more effective

A

They are the same.

194
Q

What is the main mechanism of progestin contraceptive

A

Thinning of endometrium
Thickening of cervical mucus

195
Q

What is the main mechanism of combined (estrogen and progestin) contraceptive

A

Preventing ovulation (does it every time)

196
Q

Combined oral contraceptives

A

Estrogen + Progestin
Mono bi or triphasic
Cyclic

197
Q

Cyclic combined contraceptives

A

Traditional
Take active pills for 21-24 days.
Placebo for 7-4 days
24/4 recomended over 21/7 because can use lower estrogen content

198
Q

Extended cycle combined contraceptive

A

Active pill for 84 days.
7 days of placebo.
Withdrawal bleeding every three months

199
Q

Continuous cycle combine contraceptive

A

Actie pills taken every day
No withdrawal bleeding
No medical need for menstruation with oral contraception
Write “for continuous use” on Rx

200
Q

Is natural or synthetic progesterone better on gettig past first past metabolism

A

Synthetic

201
Q

What progestins have high affinity for androgen receptors

A

Levonorgestrel
Norgestrel

202
Q

What progestins have low affinity for androgen receptors

A

Drospirenone

203
Q

What progestins have high affinity for progesterone receptors

A

All of them

204
Q

Estrogen negative feedback

A

INhibits GnRH LH and FSH.
Causing no ovulation.
Most important mechanism in combined contraceptives

205
Q

What stimulates menstrual bleeding

A

Withdrawal of progestin

206
Q

Non-contraceptive benefits of oral contraceptives

A

Reduction of dysmenorrhea
Reduction in pelvic pain from endometriosis
Reduction in premenstrual syndrome
Reduction in endometrial cancer
Reduction of acne
Reduction of hirsutism

207
Q

Venous thromboembolism

A

Blood clots
Caused by estrogen effect on clotting cascade
Caused by combined oral contraceptives

208
Q

Who should not be prescribed combined with oral contraceptive

A

35 yo smoker
CV disease
Hx of breast cancer
Migraine with aura
You CAN give these people progestin-only pill instead

209
Q

Progestin-only pill

A

Supppresses GnRH and LH

210
Q

Norethindrone

A

Older Progestin-only pill
Must be taken same time each day.
All tablets are active
Short duration of action

211
Q

Drosperinone

A

Newer Progestin-only pill
Should be taken same time each day but more forgiving because have a longer half-life.
4 placebo pills

212
Q

Drosperinone adverse affects

A

Hyperkalemia
Hyperglycemia in diabetics
Don’t give to pts with adrenal or renal problems.
Don’t give to pt with hx of cervical cancer

213
Q

Norgestrel

A

Progestin-only pill
No rx required (OTC)

214
Q

Benefits of progestin only pill

A

No weight gain
No increase in headache
Safe for CVD HTN who can’t take combined pill

215
Q

Progestin only pill adverse effects

A

Unscheduled bleeding
Increased prevalence of follicular ovarian cysts.
Drosperinone can cause hyperkalemia

216
Q

IUDs as emergency contraception

A

Copper inserted within 120 hours
Hormonal inserted within 5 days

217
Q

Plan B

A

Emergency contraceptive
Singl high does of levonorgestrel
Progestin
Must be taken within 72 hours
Less efective in women >165 lbs

218
Q

Ulipristal

A

Prescribed emergency contraception.
Binds to progesterone receptor inhibiting or delaying ovulation.
Must be taken within 5 days.
Less effective in women >195 lbs

PAS 506 (9 decks)

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