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1291 Cards in this Set
- Front
- Back
|
what is the normal total body water (TBW)?
|
60% of body weight (~40L for 70kg person)
|
|
what are the two components of extracellular fluid?
|
interstitial fluid
plasma |
|
what is the volume of ICF in a 70kg person?
|
25L
|
|
what is the volume of interstitial fluid in a 70kg person?
|
12L
|
|
what is the volume of plasma in a 70kg person?
|
3L
|
|
what are the sources of fluid entering the body?
|
food
drink oxidation |
|
in what forms does fluid leave the body?
|
urine
stool sweat respiratory |
|
what is the dominant cation in the intracellular fluid?
|
potassium
|
|
what are the dominant anions in the intracellular fluid?
|
phosphates
|
|
what is the dominant cation in the extracellular fluid?
|
sodium
|
|
what are the major anions in the extracellular fluid?
|
chloride
bicarbonate |
|
what is the difference in composition between plasma and interstitial fluid?
|
plasma contains plasma proteins
|
|
t/f... osmolality is the same for intra and extracellular fluid
|
true
|
|
hypovolaemia involves depletion of...?
|
salt and water
|
|
what are the symptoms of hypovolaemia?
|
thirst
postural dizziness weakness |
|
what are the signs of hypovolaemia?
|
postural hypotension (>10mmHg drop in systolic)
tachycardia dry mouth reduced skin turgor reduced eyeball tension reduced urine output reduced weight confusion...>stupor...>coma low JVP (not seen) |
|
what is the single most accurate marker of body water?
|
body weight
|
|
which investigation results are expected in hypovolaemia?
|
increased Hb/Hcrt
increased plasma albumin increased plasma urea increased plasma renin |
|
t/f... plasma sodium is a useful marker of hypovolaemia
|
false, concentration will usually not change but total body sodium will be low
|
|
what are the causes of hypovolaemia (sodium and water depletion)?
|
reduced Na/H2O intake
GIT losses of Na and H2O (e.g. vomiting, diarrhoea, NG tube suction, fistula) renal losses (e.g. diuretics, sodium wasting conditions - aldosterone deficiency) skin losses (e.g. excess sweating, burns) internal sequestration (e.g. peritonitis, pancreatitis, crush injuries) |
|
what are the sensors of a change in plasma volume?
|
volume receptors
pressure receptors tubular [Na] receptors |
|
what are the effector mechanisms following detection of a change in plasma volume?
|
neurohormonal (SNS, RAAS, vasopressin)
haemodynamic (fall in BP->reduced GFR) |
|
what is the net result of effector mechanisms following a reduction of plasma volume?
|
increased renal Na/H2O reabsorption
|
|
what is the treatment for hypovolaemia?
|
IV normal (isotonic) saline (150mM NaCl/0.9g%)
|
|
what is the approximate baseline requirement for Na and water?
|
150 mmol Na
2-3 L water |
|
what are the symptoms of hypervolaemia?
|
bilateral ankle swelling
breathless |
|
what are the signs of hypervolaemia?
|
oedema
raised JVP hepatomegaly ascites pulmonary oedema pleural effusion weight gain |
|
t/f... hypertension is common in acute hypervolaemia
|
false, hypertension only occurs in chronic hypervolaemia
|
|
what tests are useful to detect hypervolaemia?
|
reduced Hb/Hcrt
reduced plasma albumin CXR |
|
t/f... plasma sodium increases in hypervolaemia
|
false, excess sodium is retained with water isotonically so conc will likely remain the same
|
|
what are the causes of hypervolaemia?
|
decreased renal function (reduced GFR)
oedema disorders (CCF, cirrhosis, nephrotic syndrome) |
|
what is the treatment for hypervolaemia?
|
treat cause
salt and water restriction diuretic treatment |
|
what are the functions of the kidney?
|
regulatory - volume and composition of body fluids (includes excretion of wastes)
endocrine (erythropoietin, activated vit D, renin) |
|
how many nephrons are in one kidney?
|
1 million
|
|
what structure brings blood toward the filtering unit of the kidney?
|
afferent arteriole
|
|
what structure does an efferent arteriole carry blood away from?
|
glomerulus (tuft of capillaries surrounded by tubular collecting system)
|
|
what is the single most important measure of kidney function?
|
GFR
|
|
t/f... glomerular filtrate contains cells and proteins>50D
|
false
|
|
how much plasma fluid is filtered by glomerulus into collecting tubule?
|
1/5
|
|
t/f... 99% of filtrate in collecting tubules is reabsorbed back into plasma?
|
true
|
|
t/f... some solutes and organic substances are secreted into collecting tubules
|
true
|
|
what does the efferent arteriole branch into?
|
peritubular capillaries
|
|
express renal blood flow (RBF) in terms of cardiac output
|
RBF=1/5 x CO
|
|
what is the renal plasma flow in terms of renal blood flow?
|
~0.5 of RBF
|
|
what is the GFR in terms of renal plasma flow?
|
1/5 x RPF
|
|
what is the average GFR?
|
100mL/min
|
|
what percentage of glomerular filtration is excreted as urine?
|
1%
|
|
what is the average urine flow?
|
1mL/min
|
|
what is anuria?
|
no urine is passed
|
|
what is oliguria?
|
<400mL/day
|
|
what is polyuria?
|
>3L/day
|
|
what is a normal urine output?
|
1.5L/day
|
|
what is the name for the very metabolically active part of the loop of Henle?
|
thick ascending limb (TAL)
|
|
t/f... the late distal tubule and the cortical collecting duct have the same function
|
true
|
|
where do collecting ducts form?
|
late distal tubule
|
|
where is sodium reabsorbed?
|
65% in proximal tubule
25% TAL 6% early distal tubule 2.5% cortical collecting duct 1% medullary collecting duct |
|
how much filtered sodium is reabsorbed?
|
99.5%
|
|
how much filtered sodium is contained in final urine?
|
0.5%
|
|
what is the fractional excretion of Na?
|
0.5%
|
|
how does sodium move from filtered urine to cell in the proximal tubule?
|
paracellularly
sodium glucose cotransporter NHE3 |
|
what does NHE3 do?
|
exchanges Na for H
|
|
what is the main mode of proximal tubule sodium reabsorption?
|
shunt (between cells)
|
|
t/f... sodium and water are reabsorbed isotonically in the proximal tubule
|
true
|
|
how is filtered sodium reabsorbed in the thick ascending limb?
|
NaK/2Cl cotransporter
|
|
t/f... no water crosses at the thick ascending limb of loop of Henle
|
true
|
|
where is sodium reabsorbed with a Cl?
|
early distal tubule
|
|
t/f... the early distal tubule is water permeable
|
false, it is water-impermeable
|
|
what is the approximate size of a kidney?
|
10 x 5 x 2.5cm
|
|
t/f... the kidneys are retroperitoneal, in the paravertebral gutters
|
true
|
|
which three muscles are related posteriorly to the kidneys?
|
psoas major
quadratus lumborum aponeurosis of transversus abdominis |
|
t/f... the left kidney is slightly lower than the right
|
false, the right kidney is lower than the left because of the liver
|
|
the anterior surfaces of the kidney face slightly...?
|
laterally
|
|
which nerves do the kidneys lie on?
|
subcostal
iliohypogastric ilioinguinal |
|
what surrounds the kidney?
|
fat and fascia
|
|
where is perinephric fat located?
|
between kidney and renal fascia
|
|
t/f... the anterior and posterior layers of the renal fascia are closely connected inferiorly
|
false
|
|
what structure gives rise to the ureter?
|
renal pelvis
|
|
what is the space deep to the renal hilum?
|
renal sinus
|
|
what is the most anterior structure of the renal hilum?
|
renal vein
|
|
t/f... the left renal vein is longer than the right renal vein
|
true
|
|
which two veins drain into the left renal vein?
|
left suprarenal vein
left gonadal vein |
|
how does inflammation affect the renal capsule?
|
capsule will be more adherent to kidney
|
|
what does the renal vein travel between in the nutcracker space?
|
superior mesenteric artery and aorta
|
|
where do the right suprarenal and gonadal veins drain?
|
directly into IVC
|
|
what are the structures of the kidney that extend inward from the cortex between the pyramids?
|
renal columns
|
|
what is the collective term for the pyramids of the kidney?
|
medulla
|
|
what is contained in the renal sinus?
|
fat and collecting system
|
|
what is the name for the opening at the renal papilla?
|
minor calyx
|
|
what do the major calyces join to form?
|
renal pelvis
|
|
t/f... there are no anastomoses between segmental renal arteries
|
true
|
|
at what level do the renal arteries leave the abdominal aorta?
|
LV2
|
|
what is the lymphatic drainage of the kidney?
|
lateral aortic (lumbar) nodes
|
|
which four muscles are related posteriorly to the kidney?
|
diaphragm
psoas major quadratus lumborum transversus abdominis |
|
which ribs are the kidneys related to?
|
right - R12
left - R11 & R12 |
|
what are the anterior relationships common to both kidneys?
|
suprarenal glands
small bowel colon |
|
what are the anterior relationships of the right kidney?
|
suprarenal gland
colon jejunum/ileum duodenum liver |
|
what are the anterior relationships of the left kidney?
|
suprarenal gland
colon jejunum stomach spleen pancreas |
|
t/f... the gallbladder is related anteriorly to the right kidney
|
false, the gallbladder rests in front of duodenum and is not in contact with right kidney
|
|
where does the ureter start?
|
where the renal pelvis narrows
|
|
descibe the smooth muscle of the ureter
|
inner longitudinal
outer circular layer |
|
how long is the ureter?
|
25 cm
|
|
what crosses the ureter anteriorly in the abdominal cavity?
|
gonadal vessels
|
|
what helps to prevent reflux of urine back into ureters
|
ureters pass obliquely through bladder wall
|
|
what is the blood supply to the ureter?
|
adjacent arteries which anastamose along ureter
|
|
in females, where do the ovarian vessels pass relative to the ureter?
|
anterior
|
|
where does the ureter pass relative to the ovary?
|
posterior
|
|
where does the ureter pass relative to the uterine artery?
|
inferior (water under bridge)
|
|
what is the "bridge" over the ureter in the male?
|
ductus deferens
|
|
what are the three sites of constriction along the ureter where a ureteric stone may lodge?
|
narrowing of renal pelvis transverse process L2)
pelvic rim (SI joint) passage through wall of bladder (medial to ischial spine) |
|
what type of pain is associated with ureteric stones?
|
ureteric colic
|
|
what is the result of obstruction of upper part of ureter?
|
hydronephrosis
|
|
what is the result of obstruction of lower part of ureter?
|
hydroureter and hydronephrosis
|
|
where does ureteric pain occur?
|
loin to groin
|
|
where does urinary bladder pain refer?
|
suprapubic
sacral |
|
where do kidneys start their development?
|
pelvic cavity
|
|
why is a horseshoe kidney low?
|
can't pass up beyond SMA
|
|
t/f... the empty bladder in an adult is entirely within pelvic cavity
|
true
|
|
t/f... an empty bladder in a neonate lies entirely in pelvic cavity
|
false, it is abdominal in children until after puberty
|
|
what is the lowest point of the bladder?
|
neck
|
|
descibe the inner surface of the bladder
|
rugae
trigone (triangular area situated posteriorly) |
|
what is the most anterior structure in the pelvis in both sexes?
|
bladder
|
|
what are the superior relationships of the bladder in males and females?
|
male - coils of intestines
female - coils of intestines and uterus |
|
what is posterior to bladder in a female?
|
cervix and upper part of vagina
|
|
what are the lateral relations of the bladder?
|
levator ani
obturator internus |
|
what lies anterior to bladder in both males and females?
|
retropubic space and puic symphysis
|
|
what is directly behind bladder in males?
|
rectum
ductus deferens seminal vesicles |
|
what lies below the bladder in males?
|
prostate
|
|
what is the urachus?
|
fibrous remnant of allantois that connects bladder to umbilicus
|
|
how long is the female urethra?
|
4cm
|
|
what are the boundaries of the female urethra?
|
internal urethral orifice and external urethral orifice
|
|
which sphincter of the urethra is under voluntary control?
|
external urethral sphincter
|
|
where does the urethra open in a female?
|
between labia minora (vestibule)
|
|
where is the sphincter vesicae?
|
bladder neck
|
|
what are the parts of the urethra in the male?
|
preprostatic urethra
prostatic urethra membranous urethra spongy urethra |
|
where is the narrowest part of the urethra in a male?
|
tip of glans penis
|
|
where is the least dilatable part of the male urethra?
|
external urethral sphincter
|
|
where is the most dilatable part of the male urethra?
|
prostatic part
|
|
what is the normal plasma osmolality?
|
290 mmol/kg
|
|
what is the normal range for plasma osmolality?
|
285-295
|
|
what is the possible range for urine osmolality?
|
50-1200
|
|
will a concentrated urine have high or low osmolality?
|
high
|
|
where are the glomeruli located?
|
cortex
|
|
where does the loop of Henle extend?
|
into the medulla
|
|
t/f... the loop of Henle generates a gradient of tissue osmolality in medulla
|
true
|
|
what is required for passive water reabsorption from the collecting duct?
|
ADH
|
|
what triggers the presence of ADH at the collecting duct?
|
increased plasma osmolality
|
|
t/f... collecting duct can allow passive water reabsorption when ADH is present
|
true
|
|
what change in plasma osmolality triggers ADH?
|
1-2%
|
|
t/f... the descending limb of the loop of Henle is water permeable and has no active solute transport
|
true
|
|
t/f... the ascending limb is water tight and has active solute transport
|
true
|
|
where in the nephron does fluid have a lower osmolality than plasma?
|
fluid entering and in the early distal tubule
|
|
when will the minimum urine osmolality occur?
|
no ADH present
sodium continues to be reabsorbed |
|
when will maximum urine osmolality occur?
|
ADH present
|
|
what allows water to be reabsorbed from the collecting duct?
|
ADH
|
|
which solute amplifies the urine concentrating process?
|
urea
|
|
where is urea trapped when ADH is present?
|
medulla
|
|
what is the name for the capillaries supplying loop of Henle and medulla?
|
vasa recta
|
|
which factors would increase concentrating power of kidney?
|
increased length of loop
increased pump capacity of TAL decreased urine flow rate |
|
what is required to concentrate urine?
|
adequate GFR
loop action ADH |
|
what is required to dilute urine?
|
adequate GFR
loop action early distal tubule action no or zero ADH |
|
what detects changes in plasma osmoreceptors?
|
osmoreceptors
|
|
what is stimulated by osmoreceptors?
|
thirst
synthesis of ADH |
|
what is ADH?
|
peptide of 9 amino acids
|
|
what is osmotic regulation of ADH release?
|
as osmolality increases, ADH conc increases rapidly
|
|
what factors contribute to non-osmotic regulation of ADH?
|
hypovolaemia
hypotension/shock pain, nausea, stress |
|
what percentage change is required for non-osmotic regulation?
|
10%
|
|
what are the two actions of ADH?
|
H2O reabsorption
vasoconstriction |
|
where does ADH act?
|
at V2 receptors at:
cortical collecting duct medulla collecting duct |
|
what type of receptor is V2?
|
G protein coupled
|
|
what is the action of protein kinases activated by ADH?
|
cause AQP2 channels to move to apical membrane
|
|
what are the features of diabetes insipidus?
|
increased plasma osmolality
increased plasma sodium |
|
what is a diuretic?
|
an agent that increases the urine flow rate
|
|
what percentage of filtered sodium is excreted?
|
0.5%
|
|
what is the average fractional excretion of H2O?
|
1%
|
|
t/f... the major mechanism of diuresis is to increase GFR
|
false
|
|
what are the xanthines?
|
adenosine receptor blockers
|
|
what is the effect of adenosine in the afferent arteriole?
|
vasoconstriction
|
|
how do xanthines increase the GFR?
|
block adenosine receptors->vasodilation in afferent arteriole->increase GFR
|
|
which drugs achieve their diuretic effect by increasing GFR?
|
xanthines
digoxin |
|
how does digoxin increase GFR?
|
increase in CO
|
|
what is the major mechanism of diuresis?
|
decreased tubular reabsorption of sodium
|
|
how does an osmotic diuretic work?
|
decreases tubular reabsorption of a non-reabsorbable solute
|
|
at what plasma level is glucose non-reabsorbable?
|
>10 mmol/L
|
|
what substance if given IV is filtered but nor reabsorbed?
|
mannitol
|
|
when is mannitol given?
|
cerebral oedema
|
|
what is the major form of diuretic drug?
|
natriuretics
|
|
which transporter contributes to sodium reabsorption in the proximal tubule?
|
GLUT2
|
|
the amount of hydrogen secreted in the proximal tubule is equal to the amount of ... in the lumen?
|
bicarbonate
|
|
which exchanger contributes to sodium reabsorption in the proximal tubule?
|
Na/H exhanger
|
|
what makes carbonic acid (H2CO3)?
|
CO2 and H2O
|
|
what does carbonic acid dissociate into?
|
HCO3 and H
|
|
what is required for CO2 and H2O to produce carbonic acid?
|
carbonic anhydrase
|
|
what is lost in the urine with acetazolamide?
|
Na and HCO3
|
|
what condition may be treated with acetazolamide?
|
glaucoma
|
|
which transporter on the apical membrane contributes to sodium reabsorption in the thick ascending limb?
|
Na2ClK cotransporter
|
|
what causes the positive ions to move through gap junctions between TAL cells?
|
positive charge in lumen
|
|
what does frusemide inhibit?
|
Na2ClK carrier
|
|
what is the effect of frusemide on electrolyte excretion?
|
loss of sodium, chloride, potassium, calcium, magnesium
|
|
what is the net effect of frusemide?
|
hypokalaemia
alkalosis |
|
where is acid lost with frusemide treatment?
|
cortical collecting duct
|
|
how much water is reabsorbed in the TAL?
|
zero
|
|
what transporter is involved in sodium reabsorption in the early distal tubule?
|
NaCl cotransporter
|
|
which diuretics act at the early distal tubule?
|
thiazides
|
|
which diuretics are the most powerful?
|
loop diuretics (25% of sodium reabsorption occurs in the TAL cf 6% in early distal tubule)
|
|
which electrolytes are lost with thiazide administration?
|
Na, Cl, Mg, K
|
|
why is K lost in the urine with thiazides?
|
lumenal Na is swapped with K and H at the cortical collecting duct
|
|
at what point is water retained in the lumen with loop diuretics and thiazides?
|
CCD (water is trapped by cations in the lumen)
|
|
what are the complications of thiazides?
|
hyponatraemia
hypovolaemia hypokalaemia alkalosis |
|
t/f... thiazides increase calcium excretion
|
false, thiazides result in reduced calcium excretion
|
|
how does calcium enter and exit the early distal tubule cells?
|
calcium channel in apical membrane
ca/3na exchanger in basolateral membrane |
|
what cells are present in the late distal tubule and cortical collecting duct?
|
principal (2/3 of cells)
intercalated (smaller, 1/3 of cells) |
|
t/f... sodium enters the principal cell down its electrochemical gradient through a channel
|
true
|
|
t/f... sodium enters the principal cell down its electrochemical gradient through a carrier
|
false
|
|
which channel does Na enter the principal cell through?
|
epithelial sodium channel
|
|
which direction and through which channel does potassium move from the principal cell in the ED/CCD?
|
into the lumen through RoMK
|
|
what drives K secretion in the early distal tubule and the cortical collecting duct?
|
electro and chemical gradients
|
|
how is acid secreted from the intercalated cells?
|
hydrogen ATP ase
|
|
why is chloride absorbed between the cells in the LD/CCD?
|
lumen has a negative charge which drives chloride across
|
|
how is the huge sodium influx in the LD/CCD counteracted?
|
K secretion (principal cell)
H secretion (intercalated cell) Cl absorption (between cells) |
|
what stimulates the processes involved in sodium reabsorption in the LD/CCD?
|
aldosterone (upon binding to a cytoplasmic receptor)
|
|
what does amiloride do?
|
inhibits the epithelial Na channel
|
|
what losses occur with amiloride?
|
Na
Cl H2O |
|
what is retained with amiloride?
|
K and H
|
|
what is spiranolactone?
|
aldosterone antagonist (and a K-sparing diuretic)
|
|
which diuretic can be given to a patient allergic to sulphonamides?
|
ethacrynic acid (acts at TAL)
|
|
which diuretics are sulphonamides?
|
ACTZ
frusemide thiazides |
|
which diuretic is a pyrazine?
|
amiloride
|
|
which diuretic is a steroid?
|
spironolactone
|
|
what are the indications for diuretic therapy?
|
hypervolaemic states: oedema (CCF, cirrhosis, nephrotic syndrome)
hypertension other: increased blood calcium (frusemide), renal ca stones (thiazide) etc |
|
which diuretic is indicated in the oedematous conditions CCF, cirrhosis and the nephrotic syndrome?
|
thiazide or frusemide
|
|
why are diuretics relatively ineffective in chronic kidney disease?
|
these patients have a greatly reduced GFR and diuretics act on lumenal carriers
|
|
which diuretic is used to treat mild hypertension?
|
thiazide alone
|
|
which diuretic is indicated in severe hypertension?
|
thiazide in combination
|
|
what are the three categories of adverse drug reactions of diuretics?
|
physiological
metabolic miscellaneous |
|
what are the physiological complications of diuretics acting at the TAL and the early distal tubule?
|
hypovolaemia
hyponatraemia hypokalaemia hypomagnesaemia metabolic alkalosis |
|
what are the physiological complications of diuretics acting at the late distal tubule/cortical collecting duct?
|
hypovolaemia
hyponatraemia hyperkalaemia acidosis |
|
what are the metabolic complications of diuretic therapy?
|
increased glucose
increased lipids increased uric acid |
|
which diuretics are associated with metabolic complications?
|
frusemide
thiazides |
|
what are the miscellaneous complications of thiazides?
|
allergies
GIT disorders (cholecystitis, pancreatitis) erectile dysfunction |
|
which arteries perfuse the renal cortex?
|
arcuate arteries
|
|
t/f... the distal tubule abuts onto the glomerulus
|
true
|
|
what regulates sodium reabsorption?
|
volume
|
|
what regulates water reabsorption?
|
osmolality
|
|
t/f... osmolality regulation overrides volume regulation
|
false
|
|
give the formula for clearance
|
clearance=([U]xvolume)/[P]
|
|
when does clearance roughly equate to GFR?
|
if a substance is freely filtered at the glomerulus and neither reabsorbed or secreted
|
|
clearance of which substance equates to GFR?
|
creatinine
|
|
what happens to the afferent arteriole when the blood pressure is low?
|
afferent arteriole constricts
|
|
what happens to the afferent and efferent arterioles when blood pressure is high?
|
afferent arteriole dilates
efferent arteriole constricts |
|
what is the effect of angiotensin II?
|
vasoconstriction
|
|
which factors will increase the tubular reabsorption of sodium?
|
increased sympathetics tone
angiotensin II aldosterone |
|
which factors reduce the tubular reabsorption of Na?
|
increased ANF->increased dopamine
increased renal perfusion pressure->increased interstitial hydrostatic pressure renal prostaglandins |
|
what stimulates the Na-H countertransporter in the proximal tubule?
|
angiotensin II
|
|
where does ANP inhibit sodium reabsorption?
|
medullary collecting duct
|
|
where does aldosterone act to stimulate reabsorption of sodium?
|
distal tubule
|
|
what are the ECG changes of hypokalaemia?
|
T wave flattening
depression of ST segment prominent U waves |
|
what are the signs of dehydration?
|
reduced skin turgor
reduced eyeball tension loss of light reflex of tongue dry mouth |
|
what are the signs of overhydration?
|
raised JVP
tachypnoea visible apex beat ascites peripheral oedema |
|
what are the signs of hyperkalaemia?
|
weakness
cardiac changes |
|
what are the signs of uraemia?
|
anaemia
leukonychia depression of CNS peripheral neuropathy scratch marks foetor asterixis, hiccups purpura calcium deposits |
|
what conditions may result in enlarged kidneys?
|
polycystic kidney disease
obstruction/stones |
|
what sign may indicate renal artery stenosis?
|
renal bruit
|
|
how is the bladder examined?
|
palpation and percussion
|
|
where in the nephron is urine maximally concentrated?
|
tip of loop of Henle
|
|
in what situation is the collecting duct impermeable to water?
|
absence of ADH
|
|
how does ADH affect the collecting duct?
|
makes it water-permeable
|
|
what is ADH released in response to?
|
high plasma osmolality or low circulating plasma volume
|
|
what is the most common cause of oliguria?
|
volume depletion
|
|
what are the signs of volume depletion?
|
tachycardia
postural hypotension reduced skin turgor reduction in weight |
|
what are the lab test results that support a diagnosis of volume depletion?
|
urea to creatinine ratio > 80
elevated Hcrt urinary osmolality > 450 urine sodium conc <20 |
|
how is fractional excretion of sodium calculated?
|
U:P sodium/U:P creatinine
|
|
what does a fractional excretion of Na less than 1% indicate?
|
volume depletion or other pre-renal factors
|
|
what does a fractional excretion of sodium of greater than 1% indicate?
|
acute tubular necrosis
|
|
what is renal clearance?
|
volume of plasma from which a substance has been removed and excreted in the urine per unit time
|
|
what is the formula for renal clearance?
|
C[x] = U[x] x V / P[x]
|
|
give an example of a substance whose clearance is equal to the RPF?
|
para-aminohippuric acid
|
|
what is the clearance of plasma glucose within the normal range?
|
zero
|
|
why does glucose appear in the urine of diabetic patients?
|
the filtered load exceeds the tubular transport maximum
|
|
what performs protein degradation in the lumen of the GIT or in cells?
|
proteases
|
|
how do proteases degrade protein?
|
hydrolyse peptide bonds
|
|
when is protein degradation accelerated?
|
starvation
chronic disease |
|
in starvation and chronic disease, how are amino acid pools replenished?
|
protein breakdown by extracellular chemical species like TNF (cachexin)
|
|
what is the first step of amino acid deamination?
|
amino-transferase (transaminase) reaction
|
|
what are the products of a transaminase reaction?
|
keto-acid and glutamate
|
|
what is deaminated in step 2 of amino acid deamination?
|
glutamate
|
|
which coenzyme is required by aminotransferases?
|
pyridoxal phosphate
|
|
what is the major site of aminotransferase synthesis and amino acid deamination?
|
liver
|
|
what is produced when glutamate is deaminated?
|
alpha-ketoglutarate and ammonium ions
|
|
which ion contributes to hepatic encephalopathy?
|
NH4+
|
|
how are NH4+ ions eliminated?
|
urea cycle
|
|
how is urea excreted?
|
glomerular filtration in the kidney
|
|
where is urea synthesised?
|
liver
|
|
where is urea excreted?
|
kidney
|
|
t/f... patients with acute and chronic renal failure will have elevated serum urea
|
true
|
|
which amino acid donates an amino group in urea synthesis?
|
aspartate
|
|
t/f... ATP is required for urea synthesis
|
true
|
|
when does massive elevation of blood urea levels occur?
|
end-stage renal failure
|
|
what is the major extracellular buffer of H+?
|
HCO3-
|
|
what are the intracellular buffers of H+?
|
HCO3- and proteins
|
|
t/f... most buffering in respiratory conditions is extracellular
|
false, plasma CO2 is the acid of respiratory acidosis so the plasma HCO3-/CO2 cannot act as a buffer
|
|
where does compensation against metabolic acid-base disturbances occur?
|
lungs
|
|
where does compensation against respiratory acid-base disturbances occur?
|
kidney
|
|
what happens in response to metabolic acidosis?
|
medullary chemoreceptor stimulates ventilation so that blood PCO2 falls by 1 to 1.5 times the fall in HCO3
|
|
what happens in response to metabolic alkalosis?
|
ventilation is depressed to retain acid (PCO2 does not rise above 55 because hypoxic drive to respiration takes over)
|
|
t/f... in acute respiratory acidosis, the plasma HCO3- will be greater than 30
|
false, this occurs in chronic respiratory acidosis when there has been sufficient time for ammoniagenesis
|
|
what does plasma HCO3- fall to in respiratory alkalosis?
|
15-18 mmol/L
|
|
what is the renal response to acidosis?
|
increased ammoniagenesis
|
|
t/f... renal correction of acidosis by ammoniagenesis occurs immediately
|
false, enzymes must be induced so there is a lag phase (12-24 hours) and peak NH4+ excretion may not occur for up to 5 days with continuing acidosis
|
|
t/f... renal correction of metabolic alkalosis occurs rapidly
|
true
|
|
what may prevent the kidneys from correcting a metabolic acidosis?
|
concomitant dehydration
|
|
what is the mechanism of renal correction of metabolic acidosis?
|
dumping of HCO3-
|
|
what is normally the first abnormality to occur in renal failure?
|
ability of kidney to concentrate urine and retain water
|
|
how much filtered sodium is reabsorbed?
|
99%
|
|
what type of sodium imbalance usually occurs with renal failure?
|
salt and water retention
|
|
what adaptive mechanisms occur in response to hyperkalaemia?
|
increased aldosterone and Na/K ATPase activity
|
|
what is the major site for nonvolatile acid excretion?
|
kidney
|
|
how much nonvolatile acid requires excretion every day?
|
approx 1meq/kg of body weight
|
|
what are the consequences of failure to excrete phosphate?
|
acid-base disturbances
disorders of calcium metabolism |
|
what are the two mechanisms of acute tubular necrosis?
|
ischaemic
nephrotoxic |
|
which type of ATN is associated with prominent tubular epithelial cell necrosis?
|
toxic
|
|
what is the major factor in ischaemic ATN?
|
shock (systemic hypotension)
|
|
what occurs in ischaemic ATN?
|
significant reduction in renal blood flow -> reduced perfusion of cortex compared to medulla -> oliguria or anuria
|
|
t/f... urine formed in the oliguric phase of ischaemic ATN is isotonic with plasma
|
true
|
|
what are the histological changes seen in ischaemic ATN?
|
loss of brush border and flattening of epithelial cells in proximal tubules
dilation of prox and distal tubules finely granular brown casts necrosis and desquamation of individual epithelial cells destruction of tubular basement membranes mitotic activity mild interstitial oedema light chronic inflammatory cell infiltrate |
|
what are the possible mechanisms for the oliguria/anuria of ischaemic ATN?
|
tubular back-leak
tubular obstruction by casts arteriolar vasoconstriction |
|
where is cell damage most obvious with nephrotoxic ATN?
|
proximal tubules
|
|
what is rhabdomyolosis?
|
breakdown of large masses of striated muscles with the resultant leakage of myoglobin and other intracellular constituents into the bloodstream
|
|
what are the most common causes of rhabdomyolosis?
|
crush injuries
trauma exertion alcohol drugs |
|
what are the symptoms of rhabdomyolosis?
|
may be asymptomatic
muscle pain stiffness weakness |
|
what are the signs of rhabdomyolosis?
|
tender, swollen muscles with a doughy feel
black or burgundy-coloured urine |
|
what are the biochemical abnormalities of rhabdomyolosis?
|
marked elevations of creatinine kinase and other muscle enzymes
hyperkalaemia hyperphosphataemia hyperuricaemia hypocalcaemia low urea:creatinine ratio |
|
what is the pathology of rhabdomyolosis associated acute renal failure?
|
acute tubular necrosis with pigmented casts in distal tubules
|
|
how is established rhabdomyolosis managed?
|
correction of volume deficit with normal saline
alkaline diuresis maintained with saline, mannitol and bicarb dialysis once ARF is established |
|
why does hyperkalaemia need early treatment in rhabdomyolosis?
|
the associated hypocalcaemia enhances the cardiotoxicity
|
|
what are the major complications associated with haemodialysis?
|
vascular access difficulties
cardiac disease bone disease B2 microglobulin deposition malnutrition |
|
what are the major complications associated with peritoneal dialysis?
|
peritonitis
exit site infections cardiac disease malnutrition difficulties with adequate dialysis once residual renal function disappears |
|
how is digoxin excreted by the kidney?
|
filtered at the glomerulus
|
|
list some drugs that are excreted by the kidney via secretion by the proximal tubule
|
probenecid
penicillin thiazides frusemide salicylates |
|
what is the effect of renal impairment on steady state blood levels of drug?
|
it will take longer for steady state levels to be achieved
|
|
t/f... renal impairment prolongs the half life of a drug
|
true
|
|
t/f... renal impairment shortens the half life of a drug
|
false
|
|
which drugs cause pre-renal ARF?
|
ACE inhibitors
angiotensin II receptor blockers NSAIDs radiocontrast agents |
|
what dilates the afferent arteriole?
|
prostaglandins
|
|
what constricts the efferent arteriole?
|
angiotensin II
|
|
how do ACE inhibitors and ARBs affect the efferent arteriole?
|
prevent vasoconstriction
|
|
how do NSAIDs affect the afferent arteriole?
|
prevent dilation (block formation of prostaglandins)
|
|
why do non-steroidals increase blood pressure?
|
prostaglandins promote sodium loss in the loop of Henle
|
|
which drugs may cause ATN?
|
aminoglycosides
cisplatinum amphotericon |
|
which drugs may cause acute interstitial nephritis?
|
antibiotics
NSAIDs PPIs |
|
which drugs may cause post renal obstruction?
|
analgesics
methysergide HIV therapies |
|
which drugs may cause chronic kidney disease?
|
analgesics
lithium |
|
which drugs may cause the nephrotic syndrome?
|
NSAIDs
penicillamine gold captopril |
|
which receptor do ARBs target?
|
AT1a receptor
|
|
how do ACE inhibitors and ARBs lower BP?
|
reduce vasoconstriction and Na reabsorption
|
|
what are the causes of prerenal ARF?
|
intravascular volume depletion
decreased cardiac output systemic vasodilation renal vasodilation drugs |
|
what are the causes of post-renal ARF?
|
ureteral obstruction (bilateral)
bladder obstruction urethral obstruction |
|
what are the causes of intrinsic ARF?
|
ischaemic ATN
nephrotoxic ATN acute interstitial nephritis acute glomerulonephritis intratubular obstruction |
|
what might a low urinary sodium and concentrated urine indicate?
|
pre-renal ARF
|
|
what occupies the space between podocytes?
|
filtration slit and slit diaphragm
|
|
what is the main protein composing the slit diaphragm?
|
nephrin
|
|
what does the intracellular domain of nephrin interact with?
|
cytoskeletal proteins in the podocytes (podocin, NEPH1, ZO-1)
|
|
what does the extracellular domain of nephrin interact with?
|
extracellular domain of nephrin from neighbouring podocyte
|
|
what enables podocytes to contract?
|
F-actin (linked to ZO-1)
|
|
what does the ZO-1 link to in the podocyte?
|
F-actins
integrins (expressed by podocytes linking them to basement membrane) |
|
what secretes the proteins in the basement membrane?
|
podocytes
|
|
t/f... the podocyte membrane is negatively charged
|
true
|
|
what determines filtration of a substance?
|
molecular size
charge |
|
what size of a neutral substance is freely filtered?
|
<10kDa
|
|
what size of a neutral substance is the upper limit of filtration?
|
70kDa
|
|
which are more easily filtered, anions or cations?
|
cations
|
|
t/f... water is freely filtered at the glomerulus
|
true
|
|
name three solutes that are freely filtered
|
water
glucose inulin |
|
how much myoglobin is filtered?
|
75%
|
|
why is very little albumin filtered?
|
albumin is negatively charged
|
|
what stimulates contraction of glomerular mesangial cells
|
ATII
ADH growth factors endothelin |
|
what stimulates relaxation of glomerular mesangial cells?
|
ANP
NO PGE2 |
|
what is the effect of relaxation of mesangial cells?
|
increase surface area of capillaries for filtration and therefore increase filtration rate
|
|
what is the effect of contraction of mesangial cells?
|
decrease filtration rate
|
|
what are the functions of the glomerular mesangial cells?
|
contractile
secrete mesangial matrix behave like macrophages proliferation |
|
what factors determine GFR?
|
surface area for filtration
filtration membrane permeability net filtration pressure |
|
what pressures contribute to glomerular filtration pressures?
|
hydrostatic pressure in capillary (main pressure) (=55)
hydrostatic pressure in Bowman's capsule (=10) colloid osmotic pressure in capillary (=25) colloid osmotic pressure in Bowman's capsule (=0) |
|
t/f... the net filtration pressure decreases along the length of glomerular capillary
|
true
|
|
t/f... GFR is very tightly regulated at 125 ml/min
|
true
|
|
over what range of MAP will the GFR remain constant?
|
90-200 mm Hg
|
|
what happens to the afferent arteriole when the smooth muscle is stretched?
|
stretch releases intracellular calcium which causes the muscle to contract
|
|
what is the effect of an increased afferent BP on blood flow to the glomerulus?
|
blood flow is reduced due to vasoconstriction of the arteriole
|
|
what is the effect of adenosine on the afferent arteriole?
|
vasoconstriction
|
|
how does the tubuloglomerular feedback mechanism respond to increased chloride conentrations?
|
macula densa cells sense high chloride concentrations and respond by releasing adenosine which constricts the afferent arteriole, reducing the flow rate
|
|
how does the tubule sense changes in flow?
|
changes in chloride concentration
|
|
what is the response by macula densa cells to a reduced flow rate in the tubules?
|
secretion of PGE2 which causes vasodilation of the afferent arteriole and renin secretion from granular cells of juxtaglomerular apparatus
renin secretion leads to production of ATII which constricts efferent arteriole secretion of NO causing vasodilation of afferent arteriole |
|
what is Bartter's syndrome?
|
NKCC2 mutation (increased renin, vasodilation of afferent arteriole)
|
|
t/f... renal sympathetic nerve activity is low under normal circumstances
|
true
|
|
what are the effects of renal sympathetic nerve activity on the afferent arteriole?
|
vasoconstriction (via noradrenaline)
[it also increases renin secretion] |
|
what is the general feature of the nephrotic syndrome?
|
massive proteinuria
|
|
t/f... podocytes can undergo regenerative proliferation
|
false
|
|
t/f... ACE inhibitors can improve nephrin expression
|
true
|
|
how are volatile acids excreted?
|
by the lungs
|
|
what excretes nonvolatile acids?
|
kidney
|
|
what is the net acid secretion for a 70 kg person?
|
70 meq/day
|
|
what is the major acid excreted?
|
ammonium ions
|
|
t/f... under normal circumstances, the kidney dumps bicarbonate
|
false
|
|
give the equation for net acid excretion
|
net acid excretion = NH4+ + TA(H2PO4-) - HCO3-
[70 = 40 + 30 - 0) |
|
what is the main system of buffering both intracellularly and extracellularly?
|
bicarbonate
|
|
what are the systems of non-bicarbonate buffering?
|
protein
phosphate bone |
|
where is bicarbonate reabsorbed?
|
proximal tubule
|
|
what is the main titratable acid?
|
HPO42-
|
|
where is HPO42- acidified?
|
late distal/CCD
|
|
where is NH3 produced?
|
proximal tubule
|
|
where is NH3 acidified?
|
late distal/CCD
|
|
what is the net result of bicarbonate reclamation?
|
sodium and bicarbonate reabsorption
|
|
how is bicarbonate generated by the proximal tubule?
|
titratable acids and NH4+ are formed by the H from the Na/H exchanger and a new bicarb is absorbed via the Na/HCO3- transporter
|
|
where is NH3 made?
|
proximal tubule cell
|
|
where are hydrogen ions added to NH3?
|
tubular lumen
|
|
what is generated via the process of acidification of TA and NH3?
|
a new bicarbonate
|
|
how does the kidney deal with acidosis?
|
makes more ammonia (delay phase for induction of enzymes)
|
|
what are the immediate, compensatory and correction phases to metabolic acidosis?
|
buffering (intracellularly and extracellularly)
compensation via ventilation renal correction |
|
what are the three phases of defence against acid-base disorders?
|
buffering
compensation correction |
|
what is the range for pCO2?
|
35-45
|
|
what is the range for pH?
|
7.35 - 7.45
|
|
what is the range for HCO3-?
|
24-28
|
|
what is the normal range for pO2?
|
80 - 100
|
|
how much acid is immediately buffered in metabolic acidosis?
|
50% of acid load
|
|
what is required for compensation of metabolic acidosis?
|
ventilation
tissue perfusion |
|
give the A-a gradient equation?
|
A-a gradient = FiO2 - pO2 - pCO2x1.2
|
|
what should the A-a gradient be below?
|
15
|
|
what may cause an inadequate renal correction of metabolic acidosis?
|
renal failure
renal tubular acidosis |
|
what is the equation for the plasma anion gap?
|
Na + K - Cl - HCO3
|
|
what should the plasma anion gap be?
|
15 +/- 4
|
|
what may a normal plasma anion gap in metabolic acidosis indicate?
|
bicarbonate loss from bowel or kidney
|
|
what may a raised plasma anion gap indicate?
|
increased load of acid (endogenous or exogenous)
reduced excretion (renal failure) |
|
what should the osmolar gap be below?
|
15
|
|
what does a metabolic acidosis and a raised osmolar gap indicate?
|
toxic alcohol
|
|
what is the normal threshold for HCO3 reabsorption?
|
25
|
|
how does proximal RTA affect the HCO3 threshold?
|
RTA lowers the threshold so there is bicarbonate wasting
|
|
where is the defect in type 1 RTA?
|
H ATPase
|
|
what electrolyte imbalance is associated with type 1 RTA?
|
hypokalaemia
|
|
where is the defect in type 4 RTA?
|
ENaC in the principal cell
|
|
what electrolyte imbalance is associated with type 4 RTA?
|
hyperkalaemia
|
|
which type of RTA is associated with disturbed calcium metabolism?
|
type 1
|
|
how much of the load is buffered in metabolic alkalosis?
|
30%
|
|
t/f... the renal correction of metabolic alkalosis occurs slowly
|
false, it is rapid
|
|
why does the pCO2 remain less than 55 in compensation of metabolic alkalosis?
|
hypoxic drive to breathe takes over
|
|
what are the two phases of metabolic alkalosis?
|
generation
maintenance |
|
what are the main GI and renal causes of metabolic alkalosis?
|
vomiting
diuretic therapy |
|
what is the treatment of metabolic alkalosis?
|
give volume (rather than acid)
|
|
which toxins build up in the failing kidney?
|
urea
potassium phosphate acid |
|
what are the features of toxin build up in the failing kidney?
|
urea (nausea)
potassium (weakness and hearth rhythm) phosphate (itch, PTH and bone disease) acid (breathlessness and bone disease) |
|
what are the features of water retention?
|
fluid in the lungs (breathlessness)
fluid in the legs (oedema) high blood pressure |
|
what blocks tubular secretion of creatinine?
|
cimetidine
|
|
t/f... urea clearance overestimates the inulin GFR
|
false, it underestimates the GFR because there is some tubular reabsorption of urea
|
|
in what situations is a urine collection inaccurate?
|
over acute change (ARF or during recovery)
|
|
t/f... bicarbonate is freely filtered by the glomerulus
|
true
|
|
where is bicarbonate reabsorbed?
|
majority in proximal tubules
some in distal tubule |
|
where is the defect in type 2 renal tubule acidosis?
|
bicarbonate reabsorption in proximal tubule
|
|
what is the normal range for plasma potassium?
|
3.5 - 5
|
|
what effect do insulin, catecholamines and increased pH have on potassium?
|
push potassium into cells
|
|
how is potassium excreted by the body?
|
90% - urine
10% - gut |
|
how much potassium is reabsorbed in the proximal tubule?
|
65%
|
|
how much potassium is reabsorbed in the TAL?
|
25%
|
|
how much potassium is reabsorbed in the early distal tubule?
|
zero
|
|
how much potassium is secreted in the early distal tubule?
|
zero
|
|
where in the nephron is potassium secreted?
|
late distal tubule
|
|
how much potassium can be secreted in the nephron?
|
0 - 20% (variable)
|
|
what is the lowest amount of potassium to be excreted?
|
5% of filtered load
|
|
how much filtered potassium is excreted in the urine?
|
5 (on a low K diet) - 30 (on a high K diet)%
|
|
what regulates potassium secretion in the late distal/CCD?
|
lumen factors: Na delivery, flow rate, negative potential difference
blood factors: aldosterone, plasma K, increased pH |
|
how does increased dietary potassium stimulate potassium secretion?
|
increase aldosterone
increase plasma K |
|
t/f... increased plasma K directly stimulates the zona glomerulosa to release aldosterone
|
true
|
|
what directly stimulates the adrenal gland to release aldosterone?
|
increased plasma K
angiotensin II |
|
what stimulates renin secretion?
|
decreased ECFV
decreased BP |
|
what are the effects of aldosterone on the kidney?
|
decrease Na excretion
increase K secretion |
|
what are the effects of hypokalaemia?
|
skeletal muscle weakness
cardiac effects (ECG changes, ectopics) ileus (pseudoobstruction) polyuria (nephrogenic DI) renal fibrosis |
|
what are the ECG changes of hypokalaemia?
|
T wave flattened
U waves |
|
t/f... acute hypokalaemia is associated with polyuria and renal fibrosis
|
false, these changes occur with chronic hypokalaemia
|
|
what can cause redistribution of potassium into the cells?
|
insulin
adrenaline increased ECF pH |
|
what are the causes of hypokalaemia?
|
excess potassium losses (urine or GIT)
reduced intake redistribution |
|
what does hypertension associated with low blood potassium indicate?
|
tumour producing too much aldosterone
|
|
what are the causes of potassium losses in the urine?
|
diuretics
excess aldosterone others |
|
what are the causes of potassium losses in the GIT?
|
vomiting
diarrhoea |
|
what is the treatment of hypokalaemia?
|
reverse cause
replace KCl (oral or IV) amiloride |
|
what are the effects of hyperkalaemia?
|
skeletal muscle weakness
ECG changes (T wave tenting, broadening of QRS, sine wave looking) |
|
what are the causes of hyperkalaemia?
|
in vitro haemolysis
redistribution increased intake renal retention of K |
|
what factors may cause potassium to move out of cells?
|
reduced insulin
beta blockers acidosis |
|
how is hyperkalaemia treated?
|
stabilise excitable tissue (give calcium infusion)
shift potassium into cells (insulin + glucose, beta2 agonist, NaHCO3) remove K (diuretic, resonium, dialysis) |
|
which has the lower mortality, transplant or dialysis?
|
transplant
|
|
t/f... high deceased donor rates push down living donor rates
|
true
|
|
what is the mortality for living kidney donors?
|
1 in 3000
|
|
which formula estimates GFR using P(cr), age and sex?
|
MDRD formula
|
|
which formula estimates GFR using P(cr), age, weight and sex?
|
Cockroft-Gault
|
|
why does diuretic therapy cause hypokalaemia and high bicarbonate?
|
due to LD/CCD loss of K and H
|
|
t/f... the early distal tubule is a diluting segment
|
true
|
|
t/f... loop diuretics reduce both the concentrating and diluting capacity of the nephron
|
true
|
|
t/f... thiazide diuretics reduce both the concentrating and diluting capacity of the nephron
|
false, thiazides reduce the diluting capacity only
|
|
why does hyponatraemia occur with diuretic therapy?
|
plasma is diluted when water loaded because the urine diluting capacity of the nephron is impaired by the diuretic
|
|
what effect does hypokalaemia have on the membrane potential difference?
|
increases pd -> increases excitability (ectopics, ventricular arrhythmias)
|
|
how does an increased pd lead to ectopics and arrhythmias?
|
not completely understood, thought to be an increase in Na channel activity
|
|
how does high K result in asystole?
|
reduces potential difference -> (reduces Na channel activity) -> reduces excitability (slows APs -> conduction ceases)
|
|
what are the three main stimuli for renin release?
|
drop in perfusion pressure in afferent arteriole (hypotension, hypovolaemia)
sympathetic stimulation low [Na] in early distal tubule (detected by macula densa cells) |
|
what is the main site of angiotensin II production?
|
lungs
|
|
what are the actions of angiotensin II?
|
acts on adrenal gland to release aldosterone
acts on proximal tubule to increase Na reabsorption constricts arterioles |
|
what do AII and ADH retain?
|
AII - Na
ADH - water |
|
what is the main dilator of afferent arteriole?
|
prostaglandins
|
|
t/f... AII in high concentrations acts to constrict the efferent arteriole
|
false, this happens with low concentrations of AII
|
|
what is the effect of high concentrations of AII?
|
afferent arteriole vasoconstriction
mesangial contraction (net effect: reduction of GFR) |
|
what acts to constrict the afferent arteriole?
|
high conc of AII
Noradrenaline |
|
how much bicarbonate is reabsorbed in the proximal tubule?
|
100%
|
|
what are the two buffer systems (and their limits) in the nephron?
|
filtered HPO4(2-) (limited to 30 mmol H+/day)
NH3 |
|
what causes a normal anion gap metabolic acidosis?
|
loss of HCO3 (prox tubule or gut)
|
|
what causes a high anion gap metabolic acidosis?
|
gain of new H+ e.g. ketoacidosis or lactic acidosis
|
|
what contributes to the anionic charge barrier of the endothelial layer of the glomerular capillaries?
|
heparan sulphate
|
|
what are the three layers of the glomerular basement membrane?
|
lamina rara externa
lamina densa lamina rara interna |
|
what prevents albumin from being filtered at the glomerulus?
|
physical barrier (GBM)
charge barrier |
|
what type of collagen forms the GBM?
|
collagen type IV in a mesh arrangement
|
|
what controls the filtration of protein?
|
pressure
renal plasma flow protein concentration size barrier charge barrier |
|
what are the causes of proteinuria (mechanisms)?
|
increased load
increased capillary wall permeability impaired tubular reabsorption |
|
what type of casts appear in overload proteinuria?
|
granular casts (fractured when cut)
|
|
what is the most common cause of proteinuria?
|
glomerular injury
|
|
what are the common presentations of proteinuria?
|
asymptomatic
frothy urine nephrotic syndrome |
|
what are the consequences of filtration of plasma proteins?
|
loss of trace elements, hormones, vitamins
Ig loss (infection) coagulation factor losses (thromboembolism) |
|
what are the consequences of albuminuria?
|
tubular dysfunction following reabsorption
hypoalbuminaemia (increased hepatic lipoprotein synthesis -> hyperlipidaemia -> lipiduria) oedema |
|
what is the clinical effect of loss of vitamin D in the urine?
|
hypocalcaemia
|
|
what is the nephrotic sydnrome?
|
proteinuria (>3.0 gm/day)
hypoalbuminaemia oedema |
|
what is the mechanism of hypoalbuminaemia in the nephrotic syndrome?
|
urinary losses of albumin
failed hepatic synthesis |
|
what is the commonest cause of adult nephrotic syndrome?
|
membranous GN
|
|
what are the pathological features of membranous GN?
|
thickened GBM (subepithelial deposits, "spikes", "tram tracks")
|
|
what are the causes of membranous GN?
|
idiopathic
secondary (neoplasia, SLE, RA, penicillamine, gold therapy, Hep B, Hep C, syphilis, sarcoid, schistosmiasis) |
|
who has a high risk of ESRD with membranous GN?
|
nephrotic syndrome
male high serum creatinine poor response to therapy |
|
how is membranous GN treated (non-nephrotic and nephrotic)?
|
non-nephrotic: diuretics and wait 6 months
nephrotic: steroids, cyclophosphamide/chlorambucil, ACEI/ARB and statins |
|
what are the clinical features of focal and segmental glomerulosclerosis?
|
nephrotic or subacute proteinuria
reduced GFR hypertension mild haematuria |
|
what percentage of patients with focal and segmental glomerulosclerosis will have ESRD at 5 years?
|
10-50%
|
|
how is FSGS treated?
|
ACEI
|
|
what is the pathophysiology of primary FSGS?
|
toxin to visceral epithelial cells
|
|
what is the most common cause of nephrotic syndrome in children?
|
minimal change disease
|
|
what are the features of minimal change disease?
|
selective proteinuria/nephrotic sydnrome
benign urine sediment, normal serum creatinine |
|
how is minimal change disease treated?
|
empirical prednisolone
cyclophosphamide/Cyclosporin A for relapse |
|
what is the pathophysiology of MCD?
|
T cell lymphokines released and cause loss of anionic charge barrier and podocyte injury
|
|
what is seen on EM with MCD?
|
foot process fusion, no deposits
|
|
what is seen on LM and IF with MCD?
|
minimal change
|
|
what are the three conditions of proteinuria?
|
transient
orthostatic persistent |
|
how is proteinuria treated?
|
treat underlying condition
salt restriction adequate (not excessive) protein intake diuretics ACEI control HTN warfarin if thromboembolism pneumovax |
|
what type of proteinuria indicates glomerular disease?
|
albuminuria
|
|
what occurs in response to volume depletion?
|
volume receptors (in carotid sinus and aortic arch) increase sympathetic activity
vasoconstriction renal salt and water retention ADH secretion renin secretion and AII production (vasoconstriction) |
|
what occurs in response to overhydration?
|
right atrial stretch receptors release ANP which mediates an acute, corrective natriuresis
|
|
how is the nephritic syndrome characterised?
|
active urine sediment with haematuria, proteinuria, fluid retention and consequent hypertension and oedema formation
|
|
how is the nephrotic syndrome characterised?
|
oedema, hypoalbuminaemia and heavy proteinuria (>3.5g/day)
|
|
what are the usual causes of the nephrotic syndrome?
|
glomerulonephritis
diabetic nephropathy vasculitis renal amyloidosis |
|
why does hypoalbuminaemia occur in the nephrotic syndrome?
|
excessive renal protein losses
increased renal protein catabolism blunted hepatic albumin synthesis |
|
what is the mechanism of oedema in the nephrotic syndrome?
|
reduction of plasma colloid osmotic pressure due to hypoalbuminaemia
renal salt and fluid retention |
|
t/f... blood volume is usually decreased in the nephrotic syndrome
|
false, blood volume is often normal
|
|
how is oedema in CCF caused?
|
renal salt and water retention secondary to renal hypoperfusion, increased sympathetic drive, increased RAAS activity and increased proximal reabsorption of sodium
|
|
what blocks the effects of the RAA axis in pregnancy?
|
progesterone and prostaglandins
|
|
how do NSAIDs and COX II inhibitors exacerbate oedema?
|
block renal prostaglandin synthesis, thereby stimulating sodium reabsorption at the loop of Henle
|
|
what does proteinuria with or without haematuria indicate?
|
renal parenchymal disease
|
|
what does haematuria alone indicate?
|
lesion anywhere along the urinary tract
|
|
where are small molecular weight proteins reabsorbed?
|
proximal tubule
|
|
how much protein is contained in normal urine?
|
<150mg/day
|
|
what is the source of the small amount of protein seen in normal urine?
|
Tamm-Horsfall secreted by the tubule
|
|
at what concentration does a dipstick test for protein become positive?
|
300 mg/L
|
|
how much albumin might occur in normal urine?
|
up to 30 mg
|
|
how does vigorous exercise affect proteinuria?
|
it can transiently increase proteinuria
|
|
what are the three components of the normal glomerular capillary wall?
|
endothelium
glomerular basement membrane epithelial podocytes |
|
what factors determine the barrier function of the glomerular capillary wall?
|
intercapillary haemodynamics
negative charge at the epithelial surface slit pores |
|
what maintains the negative charge barrier of the glomerular capillary wall?
|
glycosaminoglycans such as heparan sulphate and sialic acid
|
|
how does vigorous exercise affect erythrocyte excretion?
|
it may increase transiently
|
|
what is the sensitivity of urine microscopy, dipstick analysis and vision for haematuria?
|
urine microscopy: 0.5x10^6/L
dipstick: 5x10^6/L naked eye: 5x10^9/L |
|
what are the common causes of non-glomerular haematuria?
|
urinary tract sepsis
calculi renal tract tumours |
|
what are the common causes of glomerular haematuria?
|
IgA disease
thin glomerular basement disease |
|
how is haematuria distinguished from reddish urine caused by free heme pigment?
|
free heme pigment: negative microscopy, positive dipstick
|
|
what is the commonest type of nephrotic syndrome occurring in children?
|
minimal change disease (followed by focal sclerosing GN)
|
|
what is the commonest cause of the nephrotic syndrome in adults?
|
membranous GN (followed by FSGN)
|
|
where does the oedema of nephrotic syndrome initally and then later occur?
|
initially - subcutaneous tissue
later - serous sacs (pleural, peritoneal fluid) |
|
what are the complications of nephrotic syndrome?
|
infections
thromboembolic disease lipid abnormalities renal failure |
|
what is the only example of direct antibody mediated damage to glomeruli?
|
anti-GBM disease (Goodpasture's disease)
|
|
how does immune complex mediated damage to the glomeruli occur?
|
via activation of complement and inflammatory pathways
|
|
what are the two diseases in which glomerular damage is due to mesangial IgA deposition?
|
IgA nephropathy
Henoch-Schonlein Purpura |
|
how does damage to the glomerulus occur in vasculitis?
|
secondary to inflammation occurring within the vascular compartment
|
|
t/f... vasculitis is associated with heavy deposition of immunoglobulin and complement seen on renal biopsy
|
false, vasculitis is associated with a "pauci-immune" pattern
|
|
what is seen on electron microscopy in minimal change nephropathy?
|
fusion of podocyte foot processes
|
|
what do the immune deposits in membranous nephropathy usually consist of?
|
IgG and complement
|
|
where are deposits usually found in membranous nephropathy?
|
subepithelial side of the basement membrane
|
|
where are deposits found in post infectious GN?
|
humps in the subepithelial area
smaller deposits in the mesangium and subendothelial areas |
|
what type of deposits occur in membranous nephropathy?
|
granular deposits
|
|
what causes the damage to the GBM in membranous nephropathy?
|
complement membrane attack complex
|
|
what forms the crescents in rapidly progressive GN?
|
proliferation of epithelial cells
|
|
t/f... rapidly progressive GN typically presents with acute renal failure
|
true
|
|
what are the most common tumours associated with membranous nephropathy?
|
carcinoma of lung, colon and melanoma
|
|
t/f... immune complexes in the glomerulus may be a normal finding
|
false, they are almost always pathological
|
|
t/f... the ductus deferens passes through the prostate
|
false
|
|
what is formed by the ductus deferens and the seminal vesicle to pass through the prostate?
|
ejaculatory duct
|
|
how much fluid is contributed by the prostate?
|
15-30%
|
|
what are the three coverings of the testes that originate from the anterior abdominal wall?
|
external oblique aponeurosis
internal oblique transversalis fascia |
|
t/f... the cremaster muscle is skeletal muscle
|
true
|
|
where do the gonadal arteries leave the aorta?
|
below the renal artery
|
|
where do the testicular veins drain?
|
right - directly into IVC
left - into left renal vein |
|
t/f... the skin of the scrotum has different lymphatic drainage to the testes
|
true
|
|
what is the lymphatic drainage of the skin of the scrotum?
|
superficial inguinal nodes
|
|
what is the lymphatic drainage of the testis?
|
lateral aortic nodes
|
|
what is the thick outer covering of the testes?
|
tunica albuginea
|
|
what are the parts of the epididymis?
|
head, body and tail
|
|
where is sperm produced in the testis?
|
walls of seminiferous tubules
|
|
where is testosterone produced in the testis?
|
interstitial cells of Leydig
|
|
what forms the scrotal septum?
|
superficial (dartos) fascia
|
|
where is the sinus of epididymis?
|
lateral recess between epididymis and testis
|
|
what is the tunica vaginalis?
|
closed serous sac on anterior surface and sides of each testis and epididymis
|
|
what are the contents of the spermatic cord?
|
ductus deferens, testicular artery, artery of ductus deferens, pampiniform plexus of veins, lymph vessels, autonomic and sensory nerves, genital branch of genitofemoral nerve (supplies cremaster)
|
|
what does the ductus deferens do?
|
carries sperm
|
|
t/f... the seminal vesicle is lateral to the vas deferens
|
true
|
|
what part of the prostate is involved in BPH?
|
transition zone
|
|
what zone of the prostate is more commonly involved in cancer?
|
peripheral zone
|
|
what is the venous drainage of the prostate?
|
mainly internal iliac vein (and internal vertebral venous plexus)
|
|
what is the venous drainage of the erectile tissue of the penis?
|
deep dorsal vein of penis passes inferior to pubic symphysis and drains to prostatic venous plexus
|
|
what comprises the root of the penis?
|
bulb and 2 crura
|
|
what comprises the body of the penis?
|
corpus spongiosum and w corpora cavernosa
|
|
what are the three bodies of erectile tissue of the penis?
|
root
body glans penis |
|
what is the arterial supply to the penis?
|
internal pudendal artery
|
|
what is the muscle covering the bulb of the penis?
|
bulbospongiosus muscle
|
|
what is the muscle covering the crura of the penis?
|
ischiocavernosus muscle
|
|
when does incontinence occur?
|
when intravesical pressure exceeds urethral closure pressure
|
|
how does detrusor overactivity differ from overactive bladder syndrome?
|
DO is a urodynamic diagnosis
OAB is a collection of symptoms |
|
what are the symptoms of detrusor overactivity?
|
motor urgency
|
|
what type of urgency occurs with a UTI?
|
sensory urgency
|
|
what is the best treatment of detruosor overactivity?
|
anticholinergics with bladder training
|
|
why is urodynamics indicated in older patients with bladder overactivity before commencement of empirical therapy?
|
they may have mixed disorders and are more sensitive to side effects
|
|
what type of cancer may mimic bladder overactivity?
|
bladder cancer
|
|
what percentage of female incontinence is due to stress incontinence?
|
30%
|
|
what is the definition of genuine stress incontinence and how is it diagnosed?
|
urethral leakage when intravesical pressure exceeds urethral closure pressure, in the absence of a bladder contraction
diagnosed by videourodynamics |
|
what is the conservative management of stress incontinence?
|
pelvic floor exercises
reduce abdominal strain (weight loss, reduce cough) |
|
what are the surgical options for stress incontinence?
|
suburethral sling
pubovaginal sling |
|
t/f... if an older patient presents with nocturnal incontinence, they have bladder overactivity until proven otherwise
|
false, they have bladder underactivity until proven otherwise
|
|
what is the major neurotransmitter involved in erection?
|
NO
|
|
what is the major substance involved in detumescence?
|
phosphodiesterases
|
|
which neurotransmitters are involved in detumescence and flaccidity?
|
noradrenaline
endothelin |
|
what are the risk factors for erectile dysfunction?
|
cardiovascular disease
diabetes mellitus smoking hypertension poor general health psychological and psychiatric disorders |
|
what are the three classifications of organic ED?
|
vasculogenic
neurogenic endocrine |
|
what are the contraindications for PDE5Is?
|
recent MI
angina during intercourse using nitrates uncontrolled arrhythmias |
|
what is the best imaging modality for evaluating renal lesions (except renal failure)?
|
CT
|
|
what is the best imaging modality for the evaluation of renal failure?
|
ultrasound
|
|
by how much does a person's risk of prostate cancer increase with a positive family history (one and two first degree relatives)?
|
one 1st degree relative - x2
two - x9 |
|
what findings on PR may indicate prostate cancer?
|
hard consistency
asymmetry nodularity |
|
how long should be left before a repeat PSA?
|
6 wks to 3 months
|
|
how long does it take for PSA to drop after infection?
|
3-6 months
|
|
t/f... PSA is highly specific but not very sensitive for prostate cancer
|
false, the converse is true
|
|
what percentage of patients with a PSA between 4 and 10 and a positive rectal examination will have prostate cancer?
|
30%
|
|
what percentage of patients with normal PSA and normal rectal examination have prosate cancer?
|
2%
|
|
t/f... PSA is a good screening test for prostate cancer
|
false
|
|
which free to total PSA ratios are a) suspicious
b) almost never malignant? |
a) <10%
b) >24% |
|
what is the positive predictive value for prostate cancer of a positive rectal exam?
|
6%
|
|
what is the positive predictive value for prostate cancer of an elevated PSA?
|
20%
|
|
what is the positive predictive value for prostate cancer of a positive rectal exam and an elevated PSA?
|
30%
|
|
what is the major side effect of transrectal ultrasound biopsies?
|
infection (risk of E coli infection about 1 in 500)
|
|
which gleason score has a better prognosis: 3 + 4 = 7 or 4 + 3 = 7?
|
3 + 4 = 7
|
|
what are the treatment options for T1 and T2 prostate cancer?
|
watchful waiting
hormonal radiotherapy radical prostatectomy |
|
which Gleason scores indicate a patient will probably die from prostate cancer (not with it)?
|
gleason score > 6
|
|
what are the complications of radical prostatectomy?
|
mortality 0.7%
impotence 30-70% incontinence 2% severe, 20% mild bladder neck stricture 5% bowel injury 1% |
|
what is removed in a radical prostatectomy?
|
bladder neck, prostate, lymph nodes, seminal vesicles
|
|
what is the mainstay of treatment for T3 and T4 prostate cancer?
|
radiotherapy
|
|
what are the complications of radiotherapy?
|
mortality 0.2%
impotence 42% incontinence 6% bladder neck stricture 5% bowel injury 2% |
|
what is the difference (in terms of complications) between radiotherapy and radical prostatectomy?
|
radiotherapy - patient develops complications gradually after surgery
radical prostatectomy - patient develops complications straight away but they gradually improve |
|
what is brachytherapy?
|
implanting radioactive seedlings into the prostate gland
|
|
what is the mainstay of treatment for advanced prostate cancer (N and M stages)?
|
androgen ablation (medical or surgical)
|
|
what is the treatment for painful mets of prostate cancer?
|
radiotherapy
strontium corticosteroids palliation |
|
when is prostate development completed?
|
week 25
|
|
where in the prostate does benign prostatic hyperplasia occur?
|
transitional zone
|
|
what are the mechanisms of increased epithelial and stromal cells in periurethral area of prostate gland that occurs in BPH?
|
epithelial and stromal cell proliferation
impaired apoptosis |
|
t/f... androgens cause BPH
|
false, there is a permissive but not causative effect
|
|
what mediates the conversion of testosterone to dihydrotestosterone in the prostate?
|
5 alpha reductase
|
|
what can cause a partial regression of BPH?
|
surgical or biochemical castration
pharmacological inhibition of 5 alpha reductase |
|
in what situations will men not develop BPH?
|
castrated before puberty
5alpha reductase deficiency |
|
what acts synergistically with DHT to produce BPH?
|
oestradiol
|
|
which cells in the prostate produce secretions?
|
epithelial cells
|
|
what percentage of men aged 60 have BPH?
|
50%
|
|
what percentage of men aged 85 have BPH?
|
100%
|
|
how many men aged 85 have BPH requiring surgery?
|
25%
|
|
t/f... the majority of men under 50 with lower urinary tract symptoms have BPH
|
false, majority have a different cause
|
|
what are the two diagnoses important to consider in men with lower urinary tract symptoms?
|
BPH
OAB |
|
what are the drug therapies for BPH?
|
herbal remedies (limited quality data)
5 alpha reductase inhibitors (finasteride, dutasteride) anti-androgens alpha blockers |
|
how much does finasteride shrink the prostate by?
|
20%
|
|
what are the effects of finasteride?
|
shrinks prostate by about 20%
modest improvement in LUTS protective benefits |
|
what improves the efficacy of 5 alpha reductase inhibitors?
|
concurrent alpha blocker therapy
|
|
what are the advantages of minimally invasive therapy for BPH?
|
better outcomes than drug treatment
low morbidity more rapid return to normal activities potential for office based treatment |
|
what are the disadvantages of minimally invasive therapy for BPH?
|
cost
only modest improvements in symptoms and flow rates high re-treatment rates no long term outcome data |
|
what are the complications of TURP?
|
bleeding (primary and secondary)
infection incontinence ED retrograde ejaculation urethral stricture recurrence |
|
what are the common causes of haematuria?
|
IgA nephropathy
thin membrane disease trauma UTI calculi neoplasia BPH urethral conditions |
|
what is the commonest malignancy in patients with haematuria?
|
transitional cell carcinoma
|
|
what is the strongest risk factor for bladder cancer?
|
smoking
|
|
what are the causes of bladder cancer?
|
cigarette smoking
exposure to aromatic amines pelvic radiation phenacetin cyclophosphamide schistosomiasis |
|
what percentage of low grade papillary cancers progress to muscle invasion?
|
2-3%
|
|
what percentage of carcinomas in situ progress to muscle invasive disease?
|
54%
|
|
t/f... BCG is recommended for low grade tumours
|
false, MMC is recommended
|
|
what is the chance of spontaneous passage of kidney stones that are:
>6mm 4-6mm <4mm? |
10%
50% 90% |
|
by how much do STIs increase the risk of acquisition and transmission of HIV?
|
by a factor of up to 10
|
|
what are the four major bacterial STIs?
|
gonorrhoea
chlamydia syphilis chancroid |
|
what are the four major viral STIs?
|
HIV
HSV HPV HBV |
|
what percentage of women with chlamydia and gonorrhoea are asymptomatic?
|
70%
|
|
in what population is chlamydia common?
|
young people
|
|
what are the major manifestations of STIs?
|
urethral discharge
vaginal discharge genital ulcers |
|
which STIs may confer infertility?
|
gonorrhoea
chlamydia |
|
what is the probability of transmitting HIV, gonorrhoea, T palladum and HPV per sexual act?
|
HIV <1%
gonorrhoea 20-50% T palladum 20-50% HPV >60% |
|
what are two physiological causes of vaginal discharge?
|
menstruation
pregnancy |
|
what are the common vaginal infections causing vaginal discharge?
|
candidiasis
bacterial vaginosis trichomoniasis |
|
what are the common cervical infections causing vaginal discharge?
|
gonorrhoea
chlamydia |
|
what are the causes of urethral discharge?
|
chlamydia
gonorrhoea mycoplasma genitalium ureaplasma urealyticum other organisms |
|
what are the common infective causes of genital ulceration?
|
genital herpes
syphilis tropical STDs candidiasis |
|
which sites are involved in chlamydia?
|
male urethra
cervix |
|
what are the complications of chlamydia?
|
PID
Fitz Hugh Curtis syndrome epididymo-orchitis reactive arthritis |
|
how is chlamydia diagnosed?
|
culture
PCR/LCR |
|
how is chlamydia treated?
|
azithromycin 1g stat or doxycycline 100 mg bd for 7-10 days
failure to respond - erythromycin 500mg tds for 14 days |
|
what are the sites involved in gonorrhoea infection?
|
male urethra
cervix anal canal throat |
|
what are the complications of gonorrhoea?
|
PID
Fitz Hugh Curtis syndrome disseminated infection epididymo-orchitis |
|
how is gonorrhoea diagnosed?
|
gram stain and culture
PCR |
|
what can cause ophthalmia nenoatorum?
|
gonorrhoea
chlamydia |
|
where is gonorrhoea resistant to penicillin?
|
urban areas
|
|
t/f... in rural areas, gonorrhoea is mostly sensitive to penicillin
|
true
|
|
how is the vaginal discharge of candidiasis typically described?
|
cheesy discharge
|
|
what conditions are associated with thrush?
|
pregnancy
diabetes |
|
what is the discharge of bacterial vaginosis?
|
frothy offensive vaginal discharge
|
|
what causes bacterial vaginosis?
|
overgrowth of anaerobic bacteria
|
|
t/f... bacterial vaginosis is sexually transmitted
|
false, it is associated with sex
|
|
what are the complications of bacterial vaginosis in pregnancy?
|
low birth weight
prematurity |
|
what are the presentations of trichomonas in men and women?
|
men - usually asymptomatic
women - frothy vaginal discharge |
|
what are the complications of genital herpes?
|
urinary retention
meningitis |
|
how is herpes diagnosed?
|
culture
PCR serology |
|
which organism causes syphilis?
|
treponema pallidum
|
|
what is the incubation period of syphilis?
|
9-90 days
|
|
t/f... T pallidum is sensitive to penicillin
|
true
|
|
which STD is associated with painful destructive ulcers?
|
chancroid
|
|
which STD is associated with transient genital ulceration and long term lymphatic involvement?
|
LGV
|
|
which STD is associated with beefy, proliferative ulcers?
|
donovanosis
|
|
what is the treatment of most tropical STDs?
|
azithromycin
|
|
where do genital warts occur?
|
anywhere on the genitals
|
|
which strains of HPV tend to cause malignancies?
|
16/18
|
|
what hormonal change occurs at the onset of the first menstrual cycle?
|
pulsatile spikes of luteinising hormone secreted from anterior pituitary
|
|
what are the phases of menstruation?
|
follicular phase
luteal phase (premenstrual phase) |
|
when in the menstrual cycle does ovulation occur?
|
day 14
|
|
what is the fixed phase of menstruation?
|
luteal phase (14 days)
|
|
what is the acceptable range for length of menstrual cycle?
|
21-35 days
|
|
what is primary amenorrhoea?
|
no menarche by age 16
|
|
what are the most common reasons for late menarche?
|
high level of exercise
low body weight genetic |
|
what is secondary amenorrhoea?
|
no menstrual periods for three months or more
|
|
what is oligomenorrhoea?
|
no period for up to three months
|
|
what hormones are involved in the follicular phase of the menstrual cycle?
|
predominantly FSH producing E2 in ovary
|
|
what is the predominant hormone involved in the luteal phase?
|
LH
progesterone |
|
when in the menstrual cycle are the hypothalamic pulses more frequent and less frequent and which hormones are associated with each frequency?
|
follicular phase - more frequent pulses favour FSH
luteal phase - less frequent - LH |
|
what is thought to switch FSH to LH production in the menstrual cycle?
|
progesterone
|
|
what are the main regulators produced by the ovary controlling gonadotrophins?
|
E2
inhibin A and B |
|
where are the inhibins made?
|
granulosa and thecal cells of mature follicle
|
|
how do FSH and LH stimulate the growth of the follicle?
|
FSH stimulates granulosa cells
LH stimulates thecal cells |
|
what is the action of FSH in the follicle?
|
convert androgens to oestrogen
|
|
what do the thecal cells produce?
|
androgens
|
|
what is the active form of oestrogen?
|
17beta estradiol (E2)
|
|
what is taken up by the granulosa cell and converted by FSH to E2?
|
androstenedione
|
|
what are the E2 and P levels at the end of a menstrual cycle?
|
low
|
|
what inhibits release of FSH and LH?
|
negative feedback of rising E2
|
|
t/f... E2 inhibits release of GnRH
|
false, it inhibits release of FSH and LH but GnRH continues to stimulate synthesis of FSH and LH which accumulates in the ant pit
|
|
what causes the LH surge?
|
high blood E2 stimulates release of accumulated LH, FSH
|
|
what stimulates ovulation?
|
LH surge
|
|
what triggers formation of corpus luteum?
|
LH
|
|
what is released by corpus luteum?
|
primarily P
E2 |
|
what is the effect of E released from granulosa usually and at ovulation?
|
usually - negative feedback on FSH
ovulation - positive feedback releasing mainly LH |
|
what is necessary to trigger and maintain LH surge?
|
GnRH
|
|
for how long must the LH surge be maintained if corpus luteum is to be formed?
|
36-48 hours
|
|
what causes the degeneration of the corpus luteum?
|
drop in LH causing a drop in P and E
|
|
what is main hormone produced in the luteal phase?
|
progesterone
|
|
what contols the pulses of GnRH?
|
progesterone
|
|
what are the three phases of the endometrial cycle?
|
proliferative
secretory menstrual |
|
what is the mechanism of dysmenorrhoea?
|
increase in free arachadonic acid
stromal cells synthesise and secrete PGF2alpha, PGE2, prostacyclin |
|
what is responsible for the expulsion of menstrual blood?
|
PGE2 stimulating myometrial contractions
|
|
what change in temperature occurs following ovulation?
|
rise in temperature after ovulation
|
|
at what age are contraceptive methods most likely to fail?
|
<20
|
|
how does the OCP affect thromboembolism risk?
|
oestrogen increases the production of clotting factors (V, VII, X)
|
|
which population of women has a 30 fold increased risk of MI?
|
smokers using OCP
|
|
t/f... pregnant women are at a higher risk of thromboembolism than women taking the OCP
|
true
|
|
what is the mechanism of action of copper-bearing IUCDs?
|
alteration of intrauterine cavity milieu (influx of migratory leukocytes - localised inflammatory process)
milieu is highly hostile to sperm migration through uterus and cervix |
|
in what situations are progestogen only OCPs used?
|
breastfeeding women
focal migraine history of thromboembolism history of MI/cardiovascular disease underlying coagulopathy (Factor V Leiden) |
|
how does hormonal contraception inhibit ovulation?
|
suppression of FSH and LH peaks
hypothalamic and pituitary effect inhibition of follicular development |
|
t/f... the treatment for herpes involves preventing the virus from entering host cells
|
false, the treatment (nucleoside analogues) acts inside the cell
|
|
what type of cells are infected by gonorrhoea bacteria?
|
polymorphonuclear cells
|
|
what aspect of gonorrhoea is a potent stimulator of inflammation?
|
LPS in cell wall
|
|
what is the incubation period of N.gonorrhoea?
|
1-14 days
|
|
which factors influence incubation?
|
loading dose
host factors presence or absence of clinical symptoms |
|
what is the risk of a female transmitting gonorrhea from an infected male?
|
~50%
|
|
what is the risk of a male transmitting gonorrhea from an infected female?
|
20-25%
|
|
what is seen on gram stain of urethral exudate with gonorrhea infection?
|
gram negative intracellular diplococci
|
|
what may appear similar to gonococci?
|
meningococci
|
|
what is the best sample from a woman to look for gonorrhoea?
|
swab of endocervix
|
|
what is the disadvantage of diagnosing gonorrhoea with PCR?
|
don't get any information about antibiotic sensitivity
|
|
what does LPS mainly interact with?
|
C3b (inactivated to iC3b)
|
|
t/f... T pallidum organisms are extremely motile
|
true
|
|
which STIs cause cervical infection?
|
chlamydia
gonnorhoea |
|
which organisms cause vaginal infection?
|
trichomonas
candida albicans |
|
what is bacterial vaginosis?
|
imbalance in concentration of normal vaginal flora
|
|
which STI has a particular association with PID?
|
chlamydia
|
|
what is Fitz Hugh Curtis syndrome?
|
perihepatitis associated with gonococcal or chlamydial PID
|
|
t/f... the risk of a tubal factor infertility increases after an episode of PID
|
true
|
|
in what type of infection are clue cells present in the vaginal discharge?
|
bacterial vaginosis
|
|
t/f... many chlamydia infections are asymptomatic
|
true
|
|
what are the clinical features of a neonate who has transmitted chlamydia during vaginal delivery?
|
conjunctivitis
pneumonitis |
|
in which age group is chlamydia commonest?
|
15-25 years
|
|
which STIs are routinely screened for in asymptomatic males and females?
|
male: gonorrhoea, chlamydia
female: gonorrhoea, chlamydia, trichomonas + endogenous conditions (bacterial vaginosis, candidiasis) male and female: syphilis, Hep B, HIV, Hep A |
|
what are the causes of urethral discharge and dysuria?
|
gonorrhoea
chlamydia T. vaginalis Mycoplasma genitalis ureaplasma urealyticum |
|
what are the causes of vaginal discharge?
|
gonorrhoea
chlamydia T. vaginalis C. albicans BV |
|
what are the causes of genital ulcers?
|
HSV
syphilis chancroid donovanosis LGV |
|
what is the best investigation for syphilis?
|
serology
|
|
what is pelvic inflammatory disease?
|
a spectrum of upper genital tract inflammatory disorders among women that includes any combination of endometritis, salpingitis, yubo-ovarian abscess and pelvic peritonitis
|
|
what causes PID?
|
infection by microorganisms that ascend from the cervix or vagina
|
|
when is the endocervical mucus plug barrier less protective?
|
menses
folliclular phase (sex steroid hormone effects) douching recent endocervical/uterine instrumentation recent IUD placement |
|
t/f... currently there are increasing rates of chlamydia infection in Australia but PID is less frequent
|
true
|
|
what are the risk factors for PID?
|
STI presence
repeat chlamydial infections young age coital frequency contraceptive use invasive procedures |
|
what are the complications of PID?
|
subfertility
ectopic pregnancies chronic pain other gynaecological morbidity |
|
t/f... gonococcal PID is more likely than chlamydial PID to result in tubal factor infertility
|
false, the opposite is true
|
|
why is chlamydial PID more likely to cause tubal factor infertility than gonococcal PID?
|
recurrent infections can result in a delayed hypersensitivity reaction with intraluminal scarring and damage
|
|
which organism is the cause of most cases of PID in Australia?
|
chlamydia
|
|
what attaches the ovary to the broad ligament?
|
mesovarium
|
|
what attaches the ovary to the uterus?
|
ovarian ligament
|
|
what attaches the ovary to the uterine tube?
|
one or more fimbriae
|
|
where do the ovaries sit in nulliparous females?
|
ovarian fossa (lateral pelvic wall between ext iliac artery and ureter)
|
|
what type of epithelium lines the outer surface of the ovary?
|
cuboidal epithelium
|
|
what contains the ovarian vessels?
|
suspensory ligament
|
|
what is the nerve supply to the ovaries?
|
plexus on ovarian artery (sympathetic from T10)
reinforced by branches of hypogastric plexus |
|
where does ovary pain refer?
|
L or R lower quadrant
(may refer to medial thigh - ovary overlies obturator nerve on side wall of pelvis) |
|
what are the parts of the uterine tube from the uterus to the ovary?
|
uterine
isthmus ampulla infundibulum fimbriae |
|
what is the opening into the peritoneal cavity from the uterine tube?
|
abdominal ostium
|
|
what is salpingitis?
|
inflammation of the uterine tube
|
|
what is the normal location of fertilisation?
|
ampulla of uterine tube
|
|
how thick are the muscular walls of the uterus?
|
1 cm
|
|
what are the internal and external os?
|
internal os - opening from cervix to uterus
external os - opening from cervix to vagina |
|
what is the perimetrium?
|
serosal covering of uterus
|
|
where does the peritoneum come off the bladder and onto the uterus?
|
at the junction of the cervix and the body of the uterus
|
|
what is the deepest pouch in the peritoneal cavity?
|
rectouterine pouch (pouch of Douglas)
|
|
what is the angle of anteversion?
|
angle between long axis of vagina and long axis of cervix
|
|
t/f... the uterus usually projects into the anterior wall of the vagina
|
true
|
|
what is it called if the uterus projects into the posterior wall of the vagina?
|
retroversion
|
|
what is the angle of anteflexion?
|
angle between cervix and body of uterus
|
|
what guides the descent of the ovary into the pelvic cavity?
|
gubernaculum
|
|
what are the remains of the gubernaculum in the female?
|
round ligament
ovarian ligament |
|
where does the round ligament lie?
|
attached to uterus below the uterine tube, passes through inguinal canal to labium majus
|
|
what is the mesosalpinx?
|
part of the broad ligament between uterine tubes and ovary
|
|
what is the part of the broad ligament beneath the round ligament?
|
mesometrium
|
|
what is the suspensory ligament?
|
peritoneum covering ovarian vessels
|
|
what provides active support of the uterus?
|
muscular support - levator ani
|
|
what provides poassive support of uterus?
|
ligaments - pubocervical. transverse cervical, uterosacral
|
|
where do the ovarian arteries arise?
|
from abdominal aorta
|
|
what does the ovarian artery supply?
|
ovary and uterine tube
|
|
where do the uterine and vaginal arteries branch from?
|
internal iliac artery
|
|
what is the blood supply to the female external genitalia including erectile tissue?
|
internal pudendal artery
|
|
what are the anterior relationships to the vagina?
|
bladder
urethra |
|
what are the posterior relationships of the vagina?
|
rectum
perineal body |
|
t/f... the labia minora contain fat
|
false
|
|
what is the most common cause of commencing end stage kidney disease therapy?
|
diabetic nephropathy (31%)
(followed by GN - 25%) |
|
what is the most common GN diagnosis?
|
IgA nephropathy
|
|
how many patients with IgA nephropathy have to go onto dialysis?
|
1/4-/1/3
|
|
what is driving the chronic renal failure epidemic?
|
diabetes
|
|
where does functional and structural adaptation to kidney injury occur?
|
undamaged nephron
|
|
what biochemical changes are usually seen in patients with chronic kidney disease?
|
Na normal
increased K, PO4, Mg decreased HCO3, Ca |
|
in what order do changes (hyperkalaemia, anaemia, hyperparathyroidism, hyperphosphataemia, acidosis) occur in CKD?
|
hyperparathyroidism
anaemia acidosis hyperkalaemia hyperphosphataemia |
|
what is the dyslipidaemia that occurs in CKD?
|
hypertriglyceridaemia
|
|
t/f... most patients with CKD will end up on dialysis
|
false
|
|
what do most patients with CKD die of?
|
cardiovascular complications
|
|
what factors are proven to contribute to progression of CKD?
|
blood pressure
proteinuria protein and phosphate in the diet |
|
What are the clinical features of PCOS?
|
Hirsutism, acne, infertility, amenorrhoea, oligomenorrhoea, dysfunctional bleeding
|
|
What is the definition of PCOS?
|
Presence of two of... clinical and/or biochem signs of hyperandrogenism; oligo and/or anovulation; appearance on ultrasound of “polycystic ovaries”; exclusion of other known causes
|
|
What are the cysts in PCOS?
|
Small, immature ovarian follicles
|
|
When should the scan be performed for diagnosis of PCOS?
|
First half of cycle
|
|
How many “cysts” are required for diagnosis of PCOS?
|
12 or more follicles measuring 2-9mm in diameter
|
|
By how much is ovarian volume increased in PCOS?
|
>10cm^2
|
|
Which cells of the follicle make oestrogen?
|
Granulosal cells
|
|
What surrounds the granulosal cells?
|
Thecal cells
|
|
What do the thecal cells do?
|
Convert cholesterol to testosterone (via progesterone)
|
|
Which follicle cells convert testosterone to oestradiol?
|
Granulosal cells
|
|
Which hormones cause thecal cells to proliferate in PCOS?
|
LH, insulin
|
|
What is the main hormone product of the follicle in PCOS?
|
Testosterone
|
|
Why is testosterone the main hormone product of the follicle in PCOS?
|
Thecal cells are more numerous in PCOS
|
|
What does the excess testosterone do in PCOS?
|
Passes through basement membrane into follicle and inhibits growth of follicle
|
|
Where are the immature follicles located in PCOS?
|
Edge of ovary
|
|
What causes the hirsutism and acne of PCOS?
|
Excess testosterone
|
|
What causes the irregular/heavy bleeding in PCOS?
|
Follicles are producing oestradiol (stimulating thickening of endometrium) but no ovulation occurs so no progesterone is released
|
|
Which hormone stimulates ovulation?
|
LH
|
|
What causes the increased LH concentration in PCOS?
|
Prolonged exposure to unopposed oestradiol – increased GnRH pulse frequency
Antenatal programming |
|
Why is the insulin concentration increased in PCOS?
|
Obesity, insulin resistance, androgen effect in utero
|
|
How is PCOS hirsutism treated?
|
Anti-androgen or 5-alpha reductase inhibitor
|
|
How is irregular/heavy bleeding treated in PCOS?
|
Progestogens or OCP
|
|
How is anovulation treated in PCOS?
|
Anti-oestrogens or aromatase inhibitor
|
|
What is a very important concern in treating PCOS with anti-androgen or 5 alpha reductase inhibitor?
|
The patient must not become pregnant as the male foetus requires testosterone for virilisation in utero
|
|
What are the side effects of clomifene citrate?
|
Hot flushes, headaches
|
|
In what percentage of patients treated with clomifene citrate is ovulation induced?
|
70%
|
|
What percentage of patients with PCOS treated with clomifene citrate achieve pregnancy?
|
30-40%
|
|
What is the second messenger involved after fertilisation?
|
Intracellular calcium
|
|
What does the rise in intracellular calcium do after fertilisation?
|
Activates cell cycle (mitosis) and causes exocytosis of cortical granules
|
|
Which cells of the morula form the trophablast?
|
Polar cells
|
|
Which cells of the morula form the inner cell mass?
|
Apolar cells
|
|
What is the difference between the polar and apolar cells of the morula?
|
Polar cells have an apical and a basolateral membrane whereas apolar cells have no differentioation between apical and basolateral membranes
|
|
What surrounds the conceptus from fertilisation to blastocyst stage?
|
Zona pellucida
|
|
What are the functions of the zona pellucida?
|
Prevents polyspermy, prevents premature implantation, prevents two zygotes from sticking together, keeps blastomeres together until compaction
|
|
What acts to impair attachment in the pre-receptive phase?
|
Epithelium has long apical microvilli, thick glycocalyx, negative charge
|
|
What happens to make the uterus receptive to implantation?
|
Apical protrusions absorb uterine fluid – decreases volume of uterine cavity, loss of negative charge, microvilli shorten, glycocalyx thins
|
|
When does attachment occur?
|
Day 6
|
|
What breaks down the zona pellucida?
|
Proteases secreted by blastocyst
|
|
What enables adherence of trophoblast cells to endometrium?
|
Adhesion molecules on both trophoblast and endometrium
|
|
When does the increase in vascularity occur after attachment?
|
Within a few hours
|
|
What happens within a few hours after attachment?
|
Increase in vascularity in stroma, formation of primary decidua, trophoblast processes invade between epithelial cells
|
|
What forms the chorion?
|
Syncitiotrophoblasts(multinuclear cells), cytotrophoblasts (proliferative cells)
|
|
What is the action of oestrogen on the uterus during attachment?
|
Oestrogen stimulates secretion LIF (leukaemia inhibitory factor) by endometrial glands, making endometrium receptive to attachment
|
|
What is the action of oestrogen on the blastocyst during attachment?
|
Stimulates release of heparin binding EGF like GF from endometrium which has actions on both blastocyst and endometrium facilitating attachment
|
|
What prevents embryo rejection?
|
Trophoblast and decidual cells produce CRH and express Fas ligand which kills activated T cells
|
|
What is the length of duration of the corpus luteum in a non-pregnant woman?
|
12-15 days
|
|
What causes luteolysis?
|
Low LH level -> fall in progesterone secretion
|
|
What is required for maternal recognition of pregnancy?
|
Prolongation of luteal phase of ovarian cycle
|
|
When is hCG secreted by trophoblasts?
|
6-7 days post-fertilisation
|
|
When is hCG measurable in the maternal circulation?
|
8-12 days
|
|
Which cells secrete hCG?
|
Syncytiotrophoblasts
|
|
What is the action of hCG in pregnancy?
|
Prevents luteolysis, maintains progesterone production
|
|
When is the corpus luteum no longer required?
|
By day 40
|
|
What takes over the function of the corpus luteum?
|
Placental trophoblasts produce progesterone, embryo produces oestrogen
|
|
When do hCG levels fall?
|
By 6-7 weeks
|
|
What do syncytiotrophoblasts start to secrete by 6-7 weeks that is important for fetal growth?
|
Somatomammatrophins
|
|
t/f... progesterone, oestrogen and placental lactogen continue to increase throughout pregnancy until birth
|
true
|
|
t/f... hCG increases throughout pregnancy
|
false, hCG levels start to fall at about 6-7 weeks and remain at a low level throughout pregnancy
|
|
what is responsible for morning sickness?
|
hCG
|
|
what are androgens?
|
A major class of steroid hormones that develop and maintain physiological masculine characteristics
|
|
What are the two androgens necessary and sufficient for physiological masculine development?
|
Testosterone and dihydrotestosterone
|
|
Which hormone induces testosterone production?
|
LH
|
|
Which pituitary hormone stimulates sperm production?
|
FSH
|
|
Where is most testosterone produced?
|
Leydig cells in testis
|
|
What is the rate-limiting step in testosterone synthesis?
|
Cholesterol side chain cleavage (first step)
|
|
At what three stages is testosterone produced at adult levels?
|
Fetal, perinatal, pubertal (->adult->ageing)
|
|
what is the production rate of testosterone in males and females/children/castrated men?
|
Male – 7.0 mg/day
Female – 0.2 mg/day |
|
How is testosterone inactivated?
|
Hepatic oxidation and conjugation; renal excretion
|
|
How is testosterone activated?
|
Reduced to DHT by 5alpha reductase (5-10%)
Converted to oestradiol by aromatase (0.2%) |
|
t/f... testosterone is more potent than DHT
|
false, DHT is more potent
|
|
what mediates most androgen effects?
|
Androgen receptor
|
|
Where is the androgen receptor gene located?
|
X chromosome
|
|
How is sensitivity of androgen receptors related to the polyglutamine tract length?
|
Short – more sensitive; longer – less sensitive [normal range: 8-35 CAG repeats]
|
|
What is the most common cause of classical hypogonadism?
|
Klinefelter’s syndrome (47 XXY)
|
|
What is the characteristic feature of Klinefelter’s syndrome?
|
Very small testes (<4ml)
|
|
What is normal testis volume?
|
>15ml
|
|
What is the frequency of Klinefelter’s?
|
1 in 650 male births
|
|
Why does hypogonadism occur in Kallmann’s syndrome?
|
Secondary failure of hypothalamic machinery
|
|
t/f...testosterone has very good oral bioavailability
|
false, testosterone has low oral bioavailability
|
|
t/f... testosterone is rapidly metabolised in the circulation
|
true
|
|
t/f... male infertility is an indication for androgen replacement therapy
|
false
|
|
what are the risks associated with androgen abuse?
|
increased CV and prostate disease
reproductive dysfunction hepatotoxicity mood and behaviour disturbance shared needle risks |
|
what is fecundity?
|
monthly probability of pregnancy
|
|
what is the fecundity of normal couples?
|
20%
|
|
what activates the oestrogen receptor?
|
oestradiol
various synthetic oestrogens oestriol |
|
what activates the progesterone receptor?
|
progesterone
various synthetic progestogens |
|
what activates the androgen receptor?
|
dihydrotestosterone
other steroids including the progestogens of the 19-nortestosterone type |
|
what are the effects of oestrogen and progesterone in breast development?
|
ductular and alveolar growth
|
|
t/f... oestrogen and progesterone act together to stimulate growth of the myometrium
|
true
|
|
where is progesterone antagonistic to oestrogen?
|
glands of endometrium
|
|
what is the action of oestrogen receptors in the glandular epithelial tissue of the endometrium?
|
stimulate cell cycle and effect proliferation
induce synthesis of more oestradiol receptors and progesterone receptors |
|
what is needed for the endometrium to become sensitive to progesterone?
|
oestrogen
|
|
what phase of the ovarian cycle coincides with the proliferative phase of the endometrium?
|
follicular phase
|
|
what are the actions of progesterone receptors in the endometrium?
|
inhibition of further synthesis of oestradiol receptors
inhibition of protein synthesis directed at cellular replication stimulation of protein synthesis directed at cellular differentiation inhibition of synthesis of progesterone receptors |
|
t/f... progesterone induces synthesis of further progesterone receptors
|
false, progesterone binding and transcription inhibits the synthesis of progesterone receptors
|
|
what happens in the secretory phase of the endometrium?
|
cessation of mitosis
subnuclear vacuolation supranuclear vacuolation glandular secretion stromal edema stromal cell decidualisation |
|
what is the effect of withdrawal of progesterone at the end of the ovarian cycle?
|
activation of endometrial lysozomes
tissue and cellular disintegration |
|
t/f... both withdrawal of progestogen and continued exposure to a progestogen cause the endometrium to break down
|
true
|
|
why does continued progesterone exposure cause endometrium breakdown?
|
progesterone receptors are exhausted and inhibited from replenishment
|
|
what will result in less bleeding at menstruation, prolonged exposure to a progestogen or early introduction of a progestogen?
|
early introduction as this has the effect of stopping proliferation early
|
|
what are the protective factors against uterine cancer?
|
OCP
alcohol progestogens |
|
what are the risk factors for uterine cancer?
|
hypertension
obesity diabetes late menopause nulliparity prolonged unopposed oestrogen exposure other cancers familial cancer syndromes PCOS |
|
what are the possible locations of leiomyomas of the uterus?
|
intramural
subserosal submucosal |
|
what is a leiomyoma?
|
benign fibroid tumour of the myometrium
|
|
in which situations will leiomyomas cause menorrhagia?
|
if large enough and/or submucosal
(usually asymptomatic) |
|
what is the most common invasive neoplasm of the female genital tract?
|
endometrial carcinoma
|
|
when does most endometrial carcinoma occur?
|
post-menopause
|
|
t/f... 80% of endometrial carcinoma patients are stage I, grade 1 or 2 at diagnosis
|
true
|
|
describe the stages of endometrial carcinoma
|
stage I - tumour confined to corpus
stage II - tumour involves cervix stage III - tumour invades serosa and/or adnexae, vaginal metastases or metastasis to pelvic and/or paraaortic nodes stage IV - tumour extended outside the true pelvis and/or has invaded through the wall of the rectum or bladder |
|
describe the grading of endometrial carcinoma
|
grade 1 - well differentiated; <5% solid
grade 2 - well differentiated; 6-50% solid grade 3 - poorly differentiated; >50% solid |
|
what is a "chocolate" cyst?
|
fibrous tissue containing altered blood
|
|
what is endometriosis?
|
endometrial glands in abnormal locations outside the uterus
|
|
what are the commonest sites for endometriosis?
|
ovaries
uterine ligaments rectovaginal septum pelvic peritoneum laparotomy scars rarely umbilicus/appendix |
|
at what age does endometriosis typically present?
|
20-40
|
|
what condition results in chocolate cysts (sub-serosal blood-filled cysts with fibrotic walls)?
|
endometriosis
|
|
what is adenomyosis?
|
endometrial glands in the myometrium
|
|
what type of ovarian tumours result in large cystic cavities?
|
epithelial
|
|
what type of ovarian tumours are mainly teratomas?
|
germ cell tumours
|
|
what are the actions of prostaglandin synthetase inhibitors?
|
inhibit synthesis of prostaglandin
interfere with myometrial binding of PGE2 |
|
how do antifibrinolytic drugs act?
|
inhibit plasminogen activator, reducing the accelerated endometrial fibrinolytic activity found in menorrhagic women
|
|
when is cyclical progestogen therapy most effective?
|
in cases of anovulatory dysfunctional uterine bleeding
|
|
how does danazol work?
|
inhibits endometrial proliferation and causes endometrial atrophy
displacement of oestrogen from receptors indirect action - reducing pituitary steroidogenesis |
|
how do GnRH agonists work to manage dysfunctional uterine bleeding?
|
induce down regulation of the pituitary with an initial agonist phase followed by exhaustion of the pituitary and hypogonadotrophic hypogonadism
|
|
why is GnRH agonist therapy limited to 6 months?
|
long term use is associated with decreasing bone mass
|
|
what reduction in menstrual loss has been shown with progestogen releasing IUDs?
|
80-90% reduction after 12 months
|
|
what are the surgical treatments for abnormal uterine bleeding?
|
hysteroscopic endometrial ablation
myomectomy hysterectomy |
|
by how much is menstrual blood loss reduced with COCP therapy?
|
40-50%
|
|
what are the symptoms of acute withdrawal of oestrogen?
|
hot flushes
night sweats insomnia poor concentration loss of short term memory lethargy depression anxiety loss of libido skin itchiness dry vagina superficial dyspareunia |
|
what percentage of endometrial ablation patients achieve complete amenorrhoea?
|
50%
|
|
by how much do prostaglandin synthetase inhibitors reduce menstrual blood loss?
|
20-40%
|
|
what hormones are present during the menstrual phase?
|
low levels of FSH, LH
|
|
which hormones are influential in the follicular/proliferative phase?
|
oestrogen
FSH LH |
|
what comprises the wall of the cervix?
|
dense collagenous connective tissue and smooth muscle
|
|
what type of epithelium lines the endocervix?
|
simple columnar epithelium
|
|
what is the result of blockage of the openings of cervical glands?
|
retention of cervical mucus and the formation of Nabothian cysts
|
|
what type of epithelium lines the vagina?
|
non-keratinised stratified squamous epithelium
|
|
t/f... Alport's is a type of glomerulonephritis
|
false
|
|
what disease causes glomerulonephritis via direct antibody mediated damage?
|
Goodpasture's disease (anti-GBM disease)
|
|
what are the two mechanisms of immune complex mediated damage in GN?
|
binding of Abs to planted Ags
deposition of circulating immune complexes in the glomerular capillaries |
|
which two disease are caused by mesangial IgA deposition?
|
IgA nephropathy
Henoch-Schonlein Purpura |
|
what causes glomerular injury in IgA nephropathy and HSP?
|
local activation of complement proteins by the deposited IgA
|
|
why do IgA nephropathy and HSP have a limited response to immunosuppressive treatment?
|
deposited IgA is polyclonal
|
|
give an example of glomerulonephritis caused by vasculitis
|
Wegener's granulomatosis
|
|
which diseases have a pauci-immune appearance on renal biopsy?
|
vasculitis mediated GN
|
|
what is the mechanism of injury in minimal change disease and FSGS?
|
disruption of glomerular function due to the production of soluble permeability factors
|
|
what is characteristic of post infectious GN?
|
IF microscopy demonstrating deposition of IgG and C3
|
|
what is the typical presentation of post infectious GN?
|
nephritic sydnrome
|
|
what is the usual presentation of IgA nephropathy?
|
episodic haematuria
|
|
what are the histological findings in Ig A nephropathy?
|
mesangial proliferation
segmental necrotising GN or rapidly progressive GN |
|
where do IgA deposits occur mainly in IgA nephropathy?
|
mainly in the mesangium (occasionally some deposits in subendothelial area)
|
|
what percentage of glomeruli are affected in focal conditions?
|
<50%
|
|
what percentage of visible glomerulus is affected in segmental conditions?
|
<70%
|
|
what are cases of primary FSGS related to?
|
minimal change nephropathy
|
|
how does FSGS usually present?
|
nephrotic range proteinuria
|
|
how does rapidly progressive (crescentic) GN present?
|
acute renal failure
|
|
what forms the crescents in rapidly progressive GN?
|
proliferation of epithelial cells resulting in the obliteration of Bowman's space and compression/collapse of the glomerulus
|
|
t/f... the GBM appears normal in minimal change nephropathy
|
true
|
|
which tumours are found in association with membranous nephropathy?
|
carcinoma of lung and colon and melanoma
|
|
where are the immune complexes found in membranous GN?
|
subepithelial side of basement membrane
|
|
how does membranous GN present?
|
nephrotic syndrome
|
|
t/f... there is little inflammatory response in membranous GN
|
true
|
|
what is seen on light microscopy in membranous GN?
|
diffuse thickening of the GBM
|
|
what do the immune deposits in membranous nephropathy consist of?
|
IgG and complement
|
|
what is probably the cause of damage to the GBM in membranous nephropathy?
|
complement membrane attack complex
|
|
what is the most common cause of immune complex deposition in membranous nephropathy?
|
in situ immune complex formation
|
|
what causes secondary hyperparathyroidism in CRF?
|
phosphate retention and decreased activation of Vitamin D
|
|
give an example of overload proteinuria
|
myeloma kidney
|
|
what is the mechanism of analgesic nephropathy?
|
tubular proteinuria (tubulointerstitial disease, failed small MW reabsorption)
|
|
how does glomerular damage cause infections?
|
filtration of plasma proteins (Ig loss, cellular immunity)
|
|
how does glomerular damage cause lipiduria?
|
hypoalbuminaemia -> increased hepatic lipoprotein synth -> hyperlipoproteinuria ->lipiduria
|
|
what are the clinical effects of loss of albumin in the urine?
|
oedema
negative nitrogen balance dyslipidaemia, platelet aggregation |
|
what is the nephrotic syndrome?
|
proteinuria (>3g/day)
hypoalbuminaemia oedema |
|
what are the renal causes of pitting oedema?
|
nephrotic syndrome
renal failure |
|
what are the causes of proteinuria?
|
glomerulonephritis (membranous, FSGS, MC, MCGN)
diabetic nephropathy HTN amyloid CRF |
|
which two forms of glomerulonephritis usually present with proteinuria?
|
membranous
MCD |
|
what is the commonest cause of adult nephrotic syndrome?
|
membranous GN
|
|
what are the pathological features of membranous GN?
|
thickened GM - subepithelial deposits, "spikes", "tram tracks"
|
|
what are the causes of membranous GN?
|
idiopathic
secondary (neoplasia - lung, colon; SLE; RA, penicillamine, gold therapy; HepB,C, syphilis; sarcoid, schistosomiasis) |
|
what is the usual presentation of FSGS?
|
nephrotic or subacute haematuria
|
|
what is the treatment of FSGS?
|
ACEI
|
|
what type of GN is associated with reduced GFR, hypertension, mild haematuria?
|
FSGS
|
|
what is the cause of primary FSGS?
|
toxin to visceral epithelial cells
|
|
what is the cause of secondary FSGS?
|
hydraulic injury e.g. reflux, IgA
|
|
what is the commonest form of GN in children?
|
minimal change disease
|
|
which stressors can cause transient proteinuria?
|
fever
exercise |
|
what is the most common cause of renal disease requiring endstage therapy?
|
diabetes (followed by GN, HTN)
|
|
how many patients are there globally with endstage kidney failure?
|
>2 million
|
|
which equation is used to define eGFR used to stage CKD?
|
MDRD
|
|
t/f... patients with ESKD experience mild acidosis
|
true
|
|
what is the most common metabolic complication among patients with CKD?
|
hyperparathyroidism (followed by anaemia, hyperkalaemia, acidosis, hyperphosphataemia)
|
|
what are the strategies to prevent kidney failure?
|
prevent overweight and obesity
physical fitness diet modification - protein, salt stop smoking |
|
which three factors govern the progression of CKD?
|
primary disease
acute reversible deterioration non-specific |
|
t/f... treatment of primary kidney disease slows the progression
|
true (for some causes), false for polycystic kidney disease
|
|
which four factors are proven to contribute to progression of CKD?
|
blood pressure
proteinuria dietary protein dietary phosphate |
|
by how much is mortality from diabetes, CKD and heart disease increased in the indigenous population?
|
diabetes 14x
CKD 8x heart disease 5x |
|
what is seen on immunofluorescence in membranous GN?
|
granular GBM deposits of IgG and C3
|
|
what is seen on LM in membranous GN?
|
thickened glomerular capillary walls +/- spikes on silver stain
|
|
what is seen on EM in membranous GN?
|
subepithelial granular deposits +/- +/- spikes
|
|
what percentage of diffuse membranous GN is idiopathic?
|
85%
|
|
what are the secondary causes of diffuse membranous GN?
|
autoimmune disease
infections drugs cancer |
|
what is the prevalence of urinary stones in males and females?
|
1:10 males
1:2 females |
|
what is the risk of recurrence of a urinary stone?
|
50%
|
|
list the type of urinary stones in order of prevalence
|
calcium (75%)
struvite (15%) uric acid (5-10%) cystine (1%) |
|
what dietary advice should be given to stone formers?
|
increased fluid intake
normal calcium intake low oxalate intake reduced salt intake |
|
what are the risk factors for urinary stone formation?
|
young onset of stone disease
family history chronic diarrhoea, malabsorption, intestinal surgery/bypass gout recurrent UTI medications (calcium, vit D supplements, vit C, sulfur, indinivir) |
|
which stone is the only one that can be dissolved?
|
uric acid stone (alkalinise urine to pH >6.5 and allopurinol)
|
|
what determines testis differentiation?
|
testis determining factor gene on the Y chromosome
|
|
what is the thick fibrous capsule surrounding the testes?
|
white tunic
|
|
what is attached to the outer surface of the white tunic surrounding the testes?
|
tunica vaginalis
|
|
which cells in the testes produce androgens?
|
interstitial (Leydig) cells
|
|
which cells in the testes secrete androgen binding protein and inhibins?
|
Sertoli cells
|
|
where does production of spermatozoa occur?
|
seminiferous tubules
|
|
what do the bulbourethral glands secrete?
|
mucous lubricant (prior to ejaculation)
|
|
which glands add secretions at ejaculation?
|
seminal vesicles
prostate |
|
what is the main storage site for spermatozoa prior to ejaculation?
|
tail of epididymis
|
|
where does the final maturation of the spermatozoa occur?
|
female tract
|
|
what are the three layers of the bladder?
|
urothelium (multilayered transitional epithelium)
muscular layer (detrusor) adventitial layer covered posteriorly by peritoneum |
|
where is the internal urethral sphincter?
|
bladder neck
|
|
which urethral sphincter is under voluntary control?
|
external urethral sphincter
|
|
where is the external urethral sphincter in males and females?
|
males - apex of prostate to membranous urethra
females - mid urethra |
|
where do pelvic parasympathetic nerves originate?
|
S2-4
|
|
where do the lumbar sympathetic nerves originate?
|
T10-L2
|
|
which plexus innervates the smooth muscle of bladder base, bladder neck and prox urethra?
|
hypogastric plexus
|
|
what is the somatic motor innervation of the lower urinary tract?
|
S2-3 via pudendal and pelvic nerves
|
|
how is awareness of bladder filling sensed?
|
stretch receptors in detrusor muscle->parasymp->sacral SC->brainstem (pontine micturition centre)->cortex
|
|
where does sensation of bladder fullness originate?
|
trigone
|
|
what mediates the sensation of bladder fullness?
|
sympathetic fibres
|
|
what mediates the sensation of urgency?
|
pudendal nerve afferents
|
|
what is responsible for co-ordinated mucturition with detrusor contraction and synchronous relaxation of the sphincter?
|
pontine micturition centre
|
|
what is the most common cause of urinary retention?
|
obstruction to bladder outlet
|
|
what goes through the prostate?
|
prostatic urethra
two ejaculatory ducts (terminal portions of vas deferens) |
|
where do the ejaculatory ducts exit the prostate?
|
verumontanum
|
|
what are the three glandular zones of the prostate?
|
central
transition peripheral |
|
where does benign prostatic hypertrophy occur?
|
transitional zone
|
|
where does most prostate cancer arise from?
|
peripheral zone
|
|
what is the blood supply to the prostate?
|
branches of the internal iliac arteries
|
|
what is the venous drainage of the prostate?
|
dorsal vein of penis
|
|
what converts testosterone into dihydro-testosterone?
|
5 alpha reductase
|
|
t/f... changes in stromal-epithelial interaction are thought to be responsible for development of benign prostatic hypertrophy
|
true
|
|
what percentage of seminal fluid volume is prostatic secretion?
|
20%
|
|
what is PSA?
|
glycoprotein which causes liquefaction of the seminal coagulum
|
|
what are the causes of elevated PSA?
|
BPH
prostate cancer infection (prostatitis, UTI) instrumentation (TURP, prostate biopsy) |
|
what are the irritative symptoms of the lower urinary tract?
|
frequency
nocturia sensation of incomplete emptying burning pain |
|
what are the obstructive symptoms of the lower urinary tract?
|
weak stream
hesitancy intermittence straining |
|
what is a normal urine flow rate?
|
> 15ml/sec
|
|
what urinary flow rate is defined as an obstruction?
|
< 10ml/sec
|
|
which stages of prostate cancer are incurable?
|
T4, N or M
|
|
t/f... prostate cancer with a stage of T3 is always incurable
|
false, it is occasionally curable
|
|
what Gleason score do most clinical prostate cancers have?
|
5-7
|
|
how does prostate cancer spread?
|
local extension
lymphatics blood |
|
where does prostate cancer spread?
|
bone
|
|
what are the common sites for bone mets of prostate cancer?
|
pelvic bone
thoraco-lumbar vertebrae ribs |
|
t/f... bone metastasis detected on bone x-rays appear as osteosclerotic areas
|
true
|
|
what is responsible for coordinated micturition?
|
pontine micturition centre
|
|
what is responsible for coordinated bladder contraction?
|
sacral centre (S2-4)
|
|
what is responsible for control of external urethral sphincter?
|
pudendal nucleus
|
|
what are the three types of incontinence?
|
stress
urge overflow |
|
what type of incontinence occurs in detrusor overactivity?
|
urge incontinence
|
|
what type of incontinence occurs with myogenic bladder dysfunction?
|
overflow incontinence
|
|
what accounts for 60% of bladder control problems seen by GPs, urologists and geriatricians?
|
detrusor overactivity
|
|
t/f... detrusor activity is present in 1/4 of men with prostatic outlet obstruction
|
true
|
|
which receptors cause contraction of the detrusor muscle?
|
M3 receptors (ACh)
|
|
what effect might anticholinergic drugs have on the bladder?
|
cause urinary retention
|
|
which processes might cause sensory urgency?
|
inflammation
infection |
|
what is the best conservative treatment of detrusor overactivity?
|
anticholinergics and bladder training
|
|
what are the risk factors for female stress incontinence?
|
age
parity prolonged 2nd stage labour pelvic floor prolapse |
|
what are the two types of genuine stress urinary incontinence?
|
urethral hypermobility
intrinsic sphincter deficiency |
|
what are the conservative treatments for stress urinary incontinence?
|
pelvic floor exercises
reduce abdominal strain |
|
what are the surgical options for stress urinary incontinence?
|
suburethral sling
pubovaginal sling |
|
t/f... drug treatments are available for female stress incontinence
|
false
|
|
what is the commonest cause of upper unrinary tract obstruction in younger patients?
|
renal calculi
|
|
what is the major neurotransmitter involved in erection?
|
NO
|
|
what substance is involved in detumescence?
|
phosphodiesterases
|
|
which neurotransmitters are involved in detumescence and flaccidity?
|
noradrenaline
endothelin |
|
what are the risk factors for erectile dysfunction?
|
cardiovascular disease
DM smoking hypertension poor general health psychological and psychiatric disorders |
|
what are the contraindications for PDE5Is?
|
recent MI
angina during intercourse using nitrates uncontrolled arrhythmias |
|
what are the familial risk factors for BPH?
|
large prostate size
earlier age of surgery |
|
what percentage of men over 60 will have microscopic changes of BPH?
|
50%
|
|
what percentage of men over 85 will have microscopic changes of BPH?
|
100%
|
|
what percentage of men over 85 have macroscopic BPH?
|
53%
|
|
what percentage of men over 85 have BPH requiring surgery?
|
25%
|
|
what IPSS scores are associated with mild, moderate and severe symptoms?
|
mild - 0-7
moderate: 8-18 severe: 19-35 |
|
which drugs reduce the size of prostate in BPH?
|
finasteride
anti-androgens |
|
which drugs used in BPH reduce the urethral resistance?
|
alpha blockers
|
|
what are finasteride and dutasteride?
|
5 alpha reductase inhibitors
|
|
what effect does finasteride have on PSA levels?
|
approximately halves PSA levels
|
|
with which alpha blocker are side effects common?
|
prazosin
|
|
which alpha blocker has relatively few side effects?
|
tamsulosin
|
|
what are the main advantages of minimally invasive therapy for BPH?
|
significantly better outcomes than drug treatment
low morbidity more rapid return to normal activities potential for office based treatment |
|
what percentage of all male cancer is prostate?
|
24%
|
|
what percentage of male cancer deaths is due to prostate cancer?
|
11%
|
|
t/f... incidence of prostate cancer is rising sharply
|
true
|
|
what free to total ratio of PSA is suspicious?
|
<10%
|
|
what free to total ratio of PSA is almost never malignant?
|
>24%
|
|
what are the age specific PSA cut offs?
|
40-49 2.5
50-59 3.5 60-69 4.5 >70 6.5 |
|
what percentage of patients screened by DRE, PSA and TRUS will be found to have cancer?
|
2-3%
|
|
what are the treatment options for painful metastases?
|
radiotherapy
strontium-89 corticosteroids palliation |
|
what is the peak age for renal colic and urolithiasis?
|
20-40
|
|
what is the recurrence rate of kidney stones without treatment at 1 year, 5 years and 10 years?
|
10%
35% 50% |
|
which dietary factors may promote renal stone formation?
|
high protein and salt intake
high purine diets vit B6 deficiency dehydration drugs |
|
which calcium stones form in acidic urine and which form in alkaline urine?
|
acidic - ca oxalate
alkaline - ca phosphate |
|
when does renal colic occur?
|
when stones produce obstruction
|
|
what is the best imaging modality for evaluating most renal lesions in adults?
|
CT
|
|
what volume of blood produces gross (frank) haematuria?
|
>1ml blood/L urine
|
|
what is the commonest type of bladder cancer?
|
transitional cell carcinomas
|
|
which causes of vaginal discharge cause a vaginal infection?
|
candidiasis
bacterial vaginosis trichomoniasis |
|
what type of discharge occurs in bacterial vaginosis?
|
frothy offensive vaginal discharge
|
|
what is the treatment of bacterial vaginosis?
|
metronidazole 2g orally stat
|
|
which strains of HPV cause genital warts?
|
HPV 6/11
|
|
by how much do STIs increase the risk of acquisition and transmission of HIV?
|
factor of up to 10
|
|
where are 90% of STIs?
|
developing world
|
|
what guides the descent to the testes through the abdominal wall into the scrotum?
|
gubernaculum
|
|
what is obliterated to form the tunica vaginalis assoicated with the testes and epididymis?
|
processus vaginalis
|
|
when do the testes descend into the scrotum?
|
7th month
|
|
what are the congenital abnormalities associated with descent of testes?
|
congenital indirect inguinal hernia through patent processus vaginalis
cyst, hydrocele incomplete descent ectopic testis |
|
what is the function of the dartos muscle?
|
thermoregulation
|
|
what are the coverings of testis and spermatic cord?
|
external spermatic fascia
cremasteric fascia and muscle internal spermatic fascia |
|
what are the layers of superficial fascia around the pelvis?
|
membranous layer (Scarpa's)
fatty layer (Camper's) |
|
what is the cremaster muscle?
|
skeletal muscle
lifts testis |
|
what is the sensory nerve supply to scrotum?
|
ant 1/3: L1 (ilioinguinal)
post 2/3: S3 (pudendal n) |
|
what does the left testicular vein join with?
|
left renal vein->IVC
|
|
what is the lymphatic drainage of the scrotum?
|
superficial inguinal nodes
|
|
what is the lymphatic drainage of the testis?
|
drains to lateral aortic nodes
|
|
where does the testicular vein originate?
|
pampiniform plexus of spermatic cord
|
|
which pampiniform plexus more commonly forms varicocele?
|
left
|
|
which spinal nerve gives sympathetic supply to testis?
|
T10
|
|
what does each lobule in the testis contain?
|
1-3 seminiferous tubules
|
|
where is sperm produced?
|
walls of seminiferous tubules
|
|
what forms the septa in the testis?
|
tunica albuginea
|
|
where does maturation of sperm occur?
|
epididymis
|
|
how long is the duct contained in the epididymis?
|
6m
|
|
what is the tunica vaginalis?
|
closed serous sac on anterior surface and sides of each testis and epididymis
|
|
what is the sinus of epididymis?
|
lateral recess between epididymis and testis
|
|
which nerve supplies cremaster muscle?
|
genitofemoral nerrve
|
|
where is the spermatic cord?
|
extends from deep inguinal ring to upper pole of testes
|
|
what is contained in the spermatic cord?
|
ductus deferens
testicular artery (and artery of ductus deferens) pampiniform plexus of veins lymph vessels autonomic and sensory nerves genital branch of genitofemoral n |
|
how long is the ductus deferens?
|
45 cm
|
|
where in the deep inguinal ring is the ductus deferens?
|
lateral to inferior epigastric artery
|
|
what forms the "bridge" over the ureter in males?
|
ductus deferens
|
|
what forms the ejaculatory duct?
|
union of dd and duct of seminal vesicle
|
|
what supports the prostate laterally?
|
levator ani muscle
|
|
how many ducts drain into prostatic urethra?
|
20-30
|
|
what is the blood supply to prostate?
|
branches of internal iliac arteries (drains to internal iliac veins)
|
|
what is the lymphatic drainage of the prostate gland?
|
internal and external iliac nodes
|
|
where is the prostatic venous plexus?
|
anterior and lateral to prostate between capsule and fascia
|
|
where does the deep dorsal vein of penis drain?
|
prostatic venous plexus
|
|
where does the deep dorsal vein of penis pass relative to pubic symphysis?
|
inferior
|
|
what effect does BPH have on the detrusor?
|
hypertrophy and development of trabeculations and diverticula
|
|
what type of cells are present in the vaginal discharge of bacterial vaginosis?
|
clue cells
|
|
what is FItz-Hugh-Curtis syndrome?
|
perihepatitis associated with gonococcal or chlamydial PID
|
|
how is vaginal acidity maintained between 4.0 and 4.5?
|
metabolism of glycogen by lactobacilli producing lactic acid
|
|
t/f... bacterial vaginosis does not cause vaginal inflammation or vaginitis
|
true
|
|
which age group has the highest rate of contraception failure?
|
<20
|
|
which phase of the menstrual cycle has a fixed length of 14 days?
|
luteal phase
|
|
faster pulses of hypothalamic pulses favour which hormone release?
|
FSH (1 in 90 mins)
|
|
slower pulses of hypothalamic pulses favour which hormone release?
|
LH (1 in 3-4 hours)
|
|
which hormones released by the ovary are the main regulators of FSH and LH?
|
E2
inhibin A (LH) and B (FSH) |
|
which hormone stimulates granulosa cells?
|
FSH
|
|
which hormone stimualates thecal cells to produce androgens?
|
LH
|
|
which hormone stimulates conversion of androgens to oestrogen?
|
FSH
|
|
what stimulates ovulation?
|
LH surge
|
|
what is the effect of oestrogen on the hypothalamus?
|
usually negative feedback predominately acting on FSH
at ovulation, positive feedback predominately releasing LH |
|
what are the phases of the endometrial cycle?
|
proliferative
secretory menstrual |
|
when is cervical mucus thin and stretchy?
|
ovulation
|
|
when is cervical mucus thick and impenetrable?
|
luteal phase
|
|
what is the average volume of ejaculate?
|
3 ml
|
|
how many sperm are contained in an average ejaculate?
|
300-400 million
|
|
what number of sperm is required for fertility?
|
above 20 million/ml
|
|
which cells form the blood-testis barrier?
|
Sertoli cells
|
|
which of Leydig and Sertoli cells have abundant smooth endoplasmic reticulum?
|
Leydig cells
|
|
where does meiosis take place in the testis?
|
adluminal compartment
|
|
how much testosterone is produced by the Leydig cells per day?
|
5-7 mg
|
|
what converts testosterone to oestradiol?
|
aromatase
|
|
which sperm production abnormalities contribute to male infertility?
|
oligozoospermia (concentration)
asthnozoospermia (motility) teratozoospermia (morphology) |
|
what is the recommended interval between collection and analysis for semen analysis?
|
less than 30 minutes
|
|
what are the general reasons a couple may be infertile?
|
problems with ovulation
problems with sperm production blockage endometriosis female age |
|
what can be used as evidence of ovulation?
|
measurement of circulating concentration of progesterone on day 21
|
|
when in the menstrual cycle does the proliferative phase occur?
|
days 6-14 (prior to ovulation)
|
|
which ovarian phase does the proliferative phase coincide with?
|
follicular phase
|
|
what increase in thickness occurs in the late proliferative phase?
|
double in thickness (5mm)
|
|
when does the secretory phase happen?
|
days 15-26 of menstrual cycle
|
|
what is the maximum thickness of the endometrium?
|
5-6mm
|
|
in which phase is histological dating more accurate?
|
secretory phase
|
|
what occurs to spiral arteries in the menstrual phase?
|
spasmodic contractions -> ischaemia->decrease in gland secretion., loss of oedema->eventually disruption of surface epithelium and rupture of blood vessels
|
|
t/f... clotting is inhibited in the menstrual phase
|
true
|
|
when does implantation occur?
|
days 6-10 post fertilisation
|
|
following implantation, what happens to trophoblast?
|
differentiates into cytotrophoblast (inner layer, mitotically active) and syncytiotrophoblast
|
|
what produces hCG after implantation?
|
syncytiotrophoblast
|
|
when is the placenta fully developed?
|
by 4 months
|
|
what are the functions of the placenta?
|
metabolism
transport endocrine functions |
|
what percentage of women of reproductive age experience heavy menstrual bleeding?
|
10-30%
|
|
what percentage of peri-menopausal women experience heavy menstrual bleeding?
|
50%
|
|
what is the triad of risk factors classically associated with endometrial cancer?
|
obesity
DM hypertension |
|
which factors are associated with decreased risk of endometrial cancer?
|
OCP
alcohol progestogens |
|
where in the ovary is progesterone converted to testosterone?
|
thecal cells
|
|
where in the ovary is testosterone converted to oestradiol?
|
granulosal cells
|
|
what are the clinical features of PCOS?
|
anovulation
hirsutism irregular/heavy bleeding |
|
what percentage of the female population has PCOS?
|
20%
|
|
which cells does LH stimulate?
|
thecal cells
|
|
which cells does FSH act on?
|
granulosa cells
|
|
which cells in the ovary produce androgens?
|
thecal cells
|
|
which cells in the follicle produce oestrogen?
|
granulosa cells
|
|
what is the function of the zona pellucida?
|
prevents polyspermy
prevents premature implantation prevents two zygotes from sticking together keeps blastomeres together until compaction |
|
when is the conceptus surrounded by zona pellucida?
|
from fertilisation to blastocyst stage
|
|
when does attachment occur?
|
day 6
|
|
what breaks down the zona pellucida?
|
proteases
|
|
when does implantation occur?
|
day 9
|
|
what effect does oestrogen have on the uterus during attachment?
|
oestrogen acts on uterus->endometrial glands secrete LIF->LIF receptors on epi and stroma->endometrium receptive to attachment
|
|
what causes luteolysis?
|
low LH level->fall in progesterone secretion->luteolysis
|
|
what prevents luteolysis is pregnancy?
|
hCG binding to LH receptors on thecal cells
|
|
what is the median age of menopause world wide? in white women from industrialised countries?
|
45-55
50-52 |
|
which factors are associated with early menopause?
|
smoking
malnutrition ill health |
|
what is premature menopause?
|
menopause before age 40
|
|
what is the earliest hormonal change in menopause?
|
increase in FSH
|
|
what effect does HRT have on bone density?
|
improves bone density and reduces risk of osteoporotic fracture
|
|
t/f... in women over 60 HRT should not be initiated for fracture prevention
|
true
|
|
t/f... oral HRT decreases the risk of VTE
|
false, increases the risk
|
|
t/f... HRT increases heart disease in younger post menopausal women
|
false
|
|
what size is an ovary?
|
3cmx1.5x1.5
|
|
which surface of the broad ligament is the ovary attached to (and how)?
|
back of broad ligament by mesovarium
|
|
what connects the ovary to the uterine tube?
|
one or more fimbriae
|
|
which is the longest part of the uterine tube?
|
ampulla
|
|
what is the normal location of fertilisation?
|
ampulla part of uterine tube
|
|
what is the usual angle of anteversion?
|
90degrees
|
|
what is the usual angle of anteflexion?
|
170 degrees
|
|
what is the broad ligament?
|
double layer of peritoneum lateral to uterus and slung from uterine tube
|
|
what are the remains of the gubernaculum in the female?
|
round ligament and ovarian ligament
|
|
what are the parts of the broad ligament?
|
mesosalpinx
mesovarium mesometrium suspensory ligament |
|
what is contained in the suspensory ligament?
|
ovarian vessels
|
|
what is the blood supply to the ovary and uterine tube?
|
ovarian artery (from aorta)
|
|
which branches of the internal iliac artery supply the female genitalia?
|
uterine artery
vaginal artery internal pudendal artery |
|
what is the venous drainage of the female erectile tissue?
|
dorsal vein of clitoris into pelvic cavity
|
