Genitourinary Flashcards
1
Q
What are the functions of the kidneys?
A
- Filter the blood to remove waste
- Regulate water, salt, acid-base
- Regulate blood pressure
- Produce hormones and enzymes
2
Q
What are the main components of a nephron, and what are their functions?
A
Renal corpuscle- mainly functions in filtrration
Proximal convoluted tubule: main function is the reabsorption of 65% of filtrate
Loop of henle: Main function is water retention
Distal convoluted tubule: Main function is salt, pH level adjustment
Collecting duct: main function is water retention
3
Q
Describe the overall structure of a renal corpuscle
A
Loops of capillary fed from an afferent arteriole, and drained by an efferent arteriole. Covered with a layer of epithelium and an epithelial capsule.
Has a vascular pole where vessels emerge, and a urinary pole where the PCT emerges
4
Q
Describe the glomerular filtration barrier
A
Made up of three major components- the endothelial layer, the glomerular basement membrane and podocytes
Makes up a physical and charge barrier
Restricts the movement of cells, albumin and other large proteins
5
Q
Describe the glomerular capillary endothelium
A
- Contains holes to permit the movement of small molecules through
- Covered with negatively charged glycocalyx to repel -vely charged proteins in the blood
6
Q
Describe the glomerular basement membrane
A
Thick, formed from collagen and proteoglycans
Has a dense core and thinner outer layers
Acts as a physical and charge barrier
7
Q
Describe podocytes and the slit membrane
A
Podocytes are adherent to the GBM, with primary processes and interdigitating processes coming off from each. They form slits linked by a slit membrane and are also covered in negatively charged glycocalyx
The slit membrane is a fine filter also covered in glycocalyx.
8
Q
What are mesangial cells?
A
Smooth muscles packed into the capillary tuft that support the shape of the tuft
They produce ECM and are involved in scarring (glomerulosclerosis)
9
Q
What is the juxtaglomerular apparatus?
A
JG cells: Modified smooth muscle cells in the wall of the afferent arteriole responsible for secreting renin.
Macula densa cells sense Na+ in filtrate conc.
Also extraglomerular mesangial cells
In response to high Na, the afferent arteriole will vasoconstrict. At lower Na, renin is released
10
Q
What is the PCT and what are its main functions?
A
A tube of cuboidal epithelium with a large brush border for increased transport
Performs pinocytosis
Has lateral processes and infoldings to increase SA
11
Q
What is the thin limb of the nephron like?
A
Thin squamous epithelium with a role in water reabsorption. The nuclei bulge into the lumen
12
Q
What are distal tubule cells and how are they arranged?
A
They are cuboidal, with interdigitating lateral processes and infoldings, like proximal tubule cells. They have no brush border as there isn’t as much to reabsorb. They don’t perform pinocytosis but do fine-tune the salt, pH and concentration of the urine.
13
Q
What is the collecting duct and how is it organised?
A
It is the final modifier of water, salt and pH of urine
Cells go from cuboidal to columnar
14
Q
What is the macroorganisation of the kidney?
A
Kidney is surrounded by a renal capsule
Made up of lobes, with cortex on the outside and medullary pyramids on the inside
Apex of medullary pyramids called renal papillae
Papillae enveloped by calyces
Cortex contains medullary rays due to nephrons
15
Q
What parts of the nephron make up each part of the kidney?
A
Cortex is renal corpuscles and portions of the P and DCTs
Medulla is collecting ducts and loops of henle
Medullary rays are straight bundles with collecting ducts and P//DCTs going to and from the medulla. These form the centre of a lobule
16
Q
What defines a lobule?
A
Collecting duct in the middle with nephrons surrounding it
17
Q
What is the vascular supply of the kidney?
A
More superficial nephrons: Renal artery –> Interlobar artery –> arcuate artery –> interlobular artery –> afferent arteriole –> tuft –> efferent arteriole –> peritubular capillaries –> interlobular vein –> arcuate vein –> interlobar vein –> renal vein
Longer nephrons: Renal artery –> Interlobar artery –> arcuate artery –> arterial vasa recta –> capilary beds around loops –> venous vasa recta –> arcuate vein –> interlobar vein –> renal vein
18
Q
What is the structure of the ureter and bladder?
A
Lied with transitional epithelium, which is folded to allow expension
Mucous membrane for lubrication, protection
Elastic CT
Smooth muscles for peristalsis
Adventitia for blood and elasticity
19
Q
How does the lining of the urethra change?
A
Starts out transitional epithelium, as in the bladder, then onto stratified columnar and stratified squamous as it leaves
20
Q
What are the main posterior wall muscles?
A
Quadratus lumborum
Iliacus
Psoas major
21
Q
Describe quadratus lumborum
A
Origin is iliac crest, inserts rib 12 and transverse processes of L1-4
Helps in brething and bending
Innervated by ant. rami of T12-L4
22
Q
Describe Iliacus
A
Origin is iliac fossa, inserts lesser trochanter with psoas
Hip flexion
Innervated by fem nerve
23
Q
Describe psoas
A
Originates T12-L5 vertebral bodies and discs, inserts lesser trochanter with iliacus
Sit ups, bending
Innervated by ant. rami of L1-4
24
Q
What vessels supply and drain the abdominal wall?
A
Aorta branches off to give 5 lumbar arteries- like the intercostals
Veins more complex
25
Why are veins more superficial than arteries? What is the exception with this?
Superficial to prevent clamping from arteries
IVC is deep to aorta, which means it can be compressed on its left side where it crosses over after forming the left common iliac.
26
Describe the supply/drainage of the kidneys
Located on top of quad lumborum
Right kidney lower- behind R12 in comparison to Left kidney behind R11-12. Ureters exit at L1/2
Supplied by renal veins and arteries, divided into upper and lower poles
Arteries come off at L1/2, with right being longer than L
Renal veins drain to IVC at L1/2, with left being 3x longer than right
Supplied by renal plexus, pain referred to flank
Lymph is para-aortic nodes at L1/2
27
Describe the placement and supply of the ureters
Exit the kidneys at Li
Extend over the surface of psoas in line with transverse processes of lumbar spine. Crosses bifurcation of common iliac artery. Enters bladder at the trigone
Can be constricted at the junction of the ureters with the renal pelvis, or as they enter the wall of the bladder
Sup 1/3 supplied by renal artery, vein and plexus
Mid 1/3 supplied by gonadal/iliac artery and vein
Inf 1/3 supplied by sup vesical artery and vein, and hypogastric plexus
Pain referred from loin to groin
Lymph is para-aortic at L1/2 to iliac nodes
28
What is the structure of the bladder and what is its supply?
Has a partial covering of peritoneum on its upper surface, lined with transitional epithelium. Muscular coat of smooth muscle called detrusor, and a sphincter vesicae . As it fills it rises into the suprapubic cavity
Supplied by sup and inf vesical arteries and drained by vesical plexus into the internal iliac
Nerves from inferior hypogastric plexus. Symp. is sacral splachnic nerves (L1/2) and para is pelvic splachnic.
Pain referred to suprapubic region
29
Describe the trigone
A triangular smooth area at the base of the bladder, with no rugae. Ureters enter and urethra exits at its points. In between uteric openings is the interuteric crest, which is the least mobile and most easily aggravated area.
30
Describe the regions of the urethra in males vs females
Females: Superficial and deep regions
Males: pre-prostatic, prostatic, membranous and spongy areas
Lymph drainage to the internal iliac nodes
31
What are the nerves of the lumbar plexus?
L1 gives iliohypogastric and ilioinguinal nerves
LI and 2 gives genitofemoral
L2 and 3 gives lateral femoral cutaneous nerve
L2-4 gives femoral and obturator
32
Describe the iliohypogastric and ilioinguinal nerves
Both from L1
IH senses lateral gluteal and pubic skin, movement of transverse abdominis and internal obliques
II senses medial thigh, root of penis or labia majora, movement of transverse abdominis and internal obliques
Emerge at lateral border of psoas and run over QL. Pierce TA
Ilioinguinial pierces internal oblique to enter inguinal canal and accompany spermatic cord through the superficial inguinal ring
33
Describe the genitofemoral nerve
Comes from L1/2
Senses scrotum or mons pubis and skin of sup ant thigh
Moves cremasteric muscle
Emerges on top of psoas
Enters spermatic cord to innervate cremaster muscle and innervate genital skin
34
Describe the lateral femoral cutaneous nerve
Comes from L2/3
Senses skin on ant lat thigh
Emerges from lateral psoas, descending across iliacus and passing under the inguinal ligament laterally
If compressed it causes bernhardt roth syndrome which is numbness of the outer thigh
35
Describe the femoral nerve
```
Comes from L2-4
Senses ant thigh and med leg
Motors pectinius, iliacus and anterior compartment
Emerges from inf lat border of psoas
Runs between iliacus and psoas
Passes under inguinal ligament to thigh
```
36
Describe the obturator nerve
Comes from L2-4
Senses skin on med thigh
Moves obturator externis and medial compt of thigh
Emerges from lower med border of psoas, passing behind common iliac arteries and lateral to internal iliac and ureters
Runs along the pelvis to exit via the obturator foramen through the obturator canal
37
What are some tricks for remembering the nerves of the lumbar plexus?
there are 2x1, 2x2 and 2x3 contributed nerves
Lateral femoral goes to the ASIS
Genitofemoral is the only one on top of psoas
Femoral is big
Obturator is the only one medial to psoas
38
Where is our water composition from in the body?
Fat holds less water than regular body tissue, so women/overweight/elderly people have the least water%, and babies have the most
The water is held mostly in the ICF, but somewhat in the ECF, where it is split between ISF and plasma
39
What is the difference between osmolarity and osmolality?
Osmolality is the number of osmotically active particles per unit weight of solvent. Units are osmoles/kg
Osmolarity is the number of osmotically active particles per litre of solution. Its units are mOsmol/L
40
What is tonicity?
The osmotic pressure that a solute exerts across a cell membrane, causing movement of water
It accounts only for osmotically active impermeable solutes, rather than all. It isn't readily measurable.
41
What is the difference in cell result if you put a cell in hypotonic, isotonic or hypertonic solutions?
Hypotonic make cells swell
Isotonic makes cells stay the same size
Hypertonic makes cells shrink
42
Describe the Gibbs-Donnan equilibrium
Charged particles separated by semi permeable membranes can fail to distribute evenly in the presence of a non-diffusibe ion.
IE if you have 10 -ve and 10 +ve ions on one side, and the same number on the other, but add 5 non-diffusible -ve ions on one side
1. Negative ions move down their conc. gradient towards the large ions, as they are relatively less concentrated. Positive ions follow the negative to balance the charge.
The competing electrical and chemical gradients mean that there is a voltage gradient at eq- the protein side is more -ve
The water will also flow to the protein side due to oncotic pressure
43
How does the cell address the gibbs-donnan equilibrium?
- They pump out osmotically active Na+ using the Na+/K+ATPase, meaning that the K+ and proteins inside can balance the Na+ outside, making the ISF and ICF isotonic.
44
What happens in hypotonic and hypertonic ECF osmolality?
In hypotonic, the cells will swell- very dangerous for the brain
In hypertonic, the cells will shrink- this is critical for survival and is regulated by altering water levels
45
What is ECF volume?
The volume of body fluid- it depends primarily on the Na+ balance. It's less maintained
46
How can ECF volume be changed due to increased Na+ consumption?
Changes in starling's forces in the plasma can lead to movement of fluid into the interstitial space, causing edema. Additionally, a higher Na+ intake over a few days causes salt excretion to lag, but water gain due to retention to maintain osmolality at increased Na+ levels.
There is a transient increase in osmolality followed by increased Na+ excretion and increased thirst. Osmolality returns to normal but at the expense of a larger ECF volume. This continues while the high Na+ diet continues. The volume returns to normal if less Na+ is ingested or a diuretic is given
As ECF increases, BP increases and natriuresis increases
47
What is the difference between glucose, saline and free water effects on the body?
Free water is cleared rapidly, saline very slowly
Glucose is metabolised to water, so infusing it will dilute all compartments
Isotonic saline temporarily expands the extracellular compartment
Hypotonic saline expands the intracellular compartments
48
What is the overall difference between osmolality and ECF volume?
Osmolality is thightly regulated by renal water handline, controlled by ADH
ECF volume is regulated variably by Na+ handling, controlled by the RAA system
49
What is the difference between starling forces in normal and kidney capillaries?
The glomerulus has a very leaky capillary tuft. There is a 10mmHg net filtration pressure, meaning that 20% of plasma volume is filtered.
50
How is the glomerular filtration rate regulated?
Mainly via changes in glomerualr BHP
- This is due to renal autoregulation keeping GFR constant over a wide range of blood pressures. It involves a feedback mechanism causing either dilation or constriction of the afferent arteriole, or constriction of the efferent arteriole
51
How can the autoregulation of glomerular BHP change the GFR?
Constriction of afferent results in decreased BHP and decreased GFR
Dilation of afferent results in increased BHP and increased GFR
Constriction of efferent results in increased BHP and increased GFR
52
What are the five mechanisms of renal autoregulation?
- RAA system causes constriction of efferent arterioles for increased GFR
- ANP causes dilation of the afferent arterioles for increased GFR
- SNS causes constriction of the afferent arterioles for reduction in GFR
- Myogenic stretch offsets pressure increases to stabilise GFR
- Tubuloglomerular feedback constricts afferent arterioles to decrease GFR
53
How does tubuloglomerular feedback work?
High GFR --> more Na+ past the macula densa --> paracrine signals --> afferent arteriole constricts
54
How does the RAA mechanism work on capillaries?
Low GFR --> less Na+ past the macula densa --> paracrine signals --> JG cells release renin --> angiotenin II --> constriction of efferent arteriole. ALSO --> aldosterone released --> Increased Na+ reabsorption --> increased BV
55
What happens when blood pressure drops in the glomerulus?
Decreased BHP --> decreased GFR--> Decreased Na+ to macula densa --> increased renin and ang II --> constriction of efferent arteriole
Myogenic response shows decreased stretch, and tubuloglomerular feedback combines with this signal to reduce the resistance of the afferent arteriole to increase hydrostatic pressure
56
What is the function of the proximal tubule?
Major site of filtrate reabsorption- takes up 2/3 of the water and ions, 100% of the glucose and 90% of the bicarbonate. Can transport things along the transcellular pathway in primary (active, atp transport) or secondary (co/anti) transport or in paracellular.
57
How are most solutes taken back up into the blood from the PCT?
Na+ gradient is established by NA/K-ATPase and an Na+ symporter takes something along its own concentration gradient. Water follows the charge by paracellular osmosis, sometimes brining things via solvent drag
58
How is bicarbonate reabsorbed in the PCT?
First, it is converted to carbonic acid, which is the converted by carbonic anydrase on the luminal cells to H2O and CO2, which freely diffuse. Once in the cytosol, CO2 is rehydrated, and taken back into the blood by basolateral transporters
59
How is bicarbonate produced in the PCT?
Glutamine is metabolised to ammonium and bicarbonate. Ammonium is secreted into the lumen by an Na/NH4X. HCO3- is transported into the blood/ Increases in ECF acidity increases HCO3- production
60
What is fanconi syndrome?
Impaired ability of the PCT to reabsorb HCO3-, Pi, amino acids, glucose and small proteins, resulting in these being excreted
61
How is chloride reabsorbed in the late PCT?
It's concentrated in the late tubule due to everything else being taken out already
It moves down its concentration paracellularly via leaky tight junctions, and the charge difference brings more Na+ with it
62
How are drugs secreted into the PCT?
Organic anion and cation secretion is important for drug, and other xenophobic agents from the blood.
They are transported into the cells by electrogenic transporters, and then out via antiporters
63
What is the overall function of the loop of henle?
Produces urine that is more concentrated or more dilute than plasma/ Concentration can vary from 50-1200 mOsm/kg water, and volume varies from 0.5 to 20L per day
64
What are the main methods of transport of each major solute in the PCT?
```
Glucose via Na+ cotransporter
Na+ via Na+ transporter
Cl- paracellular
K+ solvent drag
H2O paracellular
HCO3- via specific transport
```
65
How does water get reabsorbed in short loop nephrons?
In the thick ascending limb, Na2ClK transporters push Na+ into the ECF and K+ is removed into the tubule via ROMK transporters. The tight junctions are impermeable to water. This causes a steep Na+ hypertonic interstitial fluid. As the thin descending limp is permeable to water, water is extruded from the TDL and taken up by the ascending vasa recta. The descending vasa recta lost water during the descent, so the concentration gradient draws water out of the loop and into the vessels
66
What is the function of the early DCT?
Fine tuning the salt balance. This area is impermeable to water and actively pumps NaCl from the tubule into the ISF
67
What is gittleman syndrome?
A mutation in the NACL transporter resulting in NACl wasting, hyperaldosteronism and hypokalemic alkalation.
68
What are the two cell types in the late DCT and what are their functions?
Principal cells cause the reabsorption of Na_ via the ENaC, driving K+ secretion due to the electrical gradient
If this K+ channel is inhibited as in Liddle's syndrome, then it will cause increased ECF volume and hypertension
Diuretics cause K+ secretion by delivering more Na+ to the tubule, which can cause hypokalemia and arrhythmias
Aldosterone causes the increased functioning of ENaC and induces more of them (late phase)
Intercalated cells usually secrete H+ for the reabsorption of HCO3-, and those that aren't used give urine its acidic pH
69
What is the overall mechanism of acid regulation?
CO2 taken in via metabolism and expired in breath is converted to HCO3-, which is produced by the kidney, and H+, which is produced by metabolism and diet, and removed by the kidney. This forms a buffer system
As a result, the HCO3- is given into the blood both by being reclaimed from tubular fluid, and from production in the kidney. H+ is removed from the blood to be secreted
70
How can ammonium help with acid extrusion?
As the amount of H+ able to be secreted is limited, H+ can be attached to NH3 in order to be secreted into the urine as NH4+
71
How is water reabsorbed in the collecting duct?
Depends on ADH- at high levels, many preexisting aquaporin 2 channels are inserted into the luminal membrane, allowing water to pass through the duct and back into the plasma. In its absence, water remains in the channels.
72
How is the long loop of henle able to return water to the blood?
The passive hypothesis
Urea becomes very high in the cortical collecting duct when ADH is present, due to H2O reabsorption.
ADH increases urea and H2O permeability in the inner medulla collecting duct, allowing Urea and H2O to mvoe into the interstitium. This decreases the relative concentration of Na in the medulla.
NaCl moves out of the tip of the loop and into the interstitium by osmosis. The countercurrent by the vasa recta allows the osmotic gradient to carry water away as in the short loops.
If ADH is low, this does not happen, then interstitial urea may be above tubular urea in concentration, causing washout.
73
What is the process that occurs when the body is dehydrated?
Water deficit leads to increased ECF osmolarity which is detected by osmoreceptors. This causes increased ADH secretion from the posterior pituitary, increased H2O permeability in the collecting ducts, increased H2O reabsorption and decreased waste of H2O. Negative feedback then turns this process off.
74
Where is ADH formed and released?
Formed in the hypothalamus, released from post. pituitary
75
Describe the mechanism of ADH release
Osmoreceptors in the supraoptic and paraventricular nuclei sense high osmolarity. The medullary vasomotor centre detects decreased volume and inputs the info to the hypothalamus
Osmoreceptor neurons are cross linked. When cells shrink, they open up gates to trigger ADH APs
76
What are the stimuli that cause ADH release?
Increased plasma osmolarity by 1-2%
Decreased circulating volume by 7-10%
Non-physiological stimulation including pain, stress.drugs, cancer, pulmonary and CNS disorders
Alcohol inhibits ADH release
77
What is centralvs nephrogenic DI and how do you tell the difference?
Central is inadequate ADH being secreted, resulting from a problem with the hypo. or PP due to tumor, infection and injury- rarely hereditary. It can be treated by giving ADH
Nephrogenic occurs when the collecting tubule is insensitive to ADH, resulting in an inability to concentrate urine. It can be due to a congenital or inherited defect in V2 receptors or Aquaporin 2
Can't be treated
Difference can be told by depriving patient of water and then giving supplementary ADH
If urine becomes concentrated it's central, if not it's nephrogenic
78
What is SIADH?
Syndrome of inappropriate ADH secretion
Higher than normal ADH levels, so patient retains unncecessary water. Lower urine osmolarity. Can cause hypo-osmolal state which can cause death etc.
Cuased by injury, tumor or drugs
Water intake must be restricted
79
What factors promote renin secretion?
Low afferent arteriolar pressure or macula densa NaCl delivery
High sympathetic nervous activity
80
What are the consequences of increased renin secretion?
Angiotensin I becomes angiotensin II, which causes increased aldosterone, vasoconstriction, increased Na+ reabsorption, thirst, ADH and decreased renal blood flow, but maintaining GFR
It also causes vasodilation at AT2 receptors
81
What is the result of increased aldosterone?
Increased Na+ reabsorption in the collecting duct,resulting in increased water intake via the paracellular route
82
How do you calculate pH/[H+]?
pH is the log10 of [H+].
| [H+] is 10^pH
83
What is the difference betwen acidaemia/alkalaemia and acidosis/alkalosis? What is the normal pH level?
In the body, pH between 7.35 and 7.45 is normal
Adicaemia is a pH below 7.35
Alkalaemia is a pH above 7.45
Acidosis is a condition usually causnig pH below 7.35
Alkalosis is a condition usually causing pH above 7.45
84
What does a buffer do? What are some examples?
A buffer minimises pH change due to its ability to absorb or exude H+ ions. This is only temporary
pH = pK + log ([base]/[acid]) so when base and acid are equal, pH = pK
Examples include bicarbonate, some proteins, such as albumin, and some chemicals, such as ammonnia
85
What is the henderson-hasselbach equation?
For the buffer HCO3-
| pH = 6.74 + log (HCO3-/pCO2)
86
How does the respiratory system help to regulate body pH?
The increased CO2 pressure causes acidosis, and decreased CO2 causes alkalosis.
Low pH also causes the stimulation of ventilation.
87
What effects does a change in pCO2 have on the buffer balance?
Normally, the relative concentrations of pCO2 and bicarbonate are equal. In respiratory acidosis, pCO2 increases, and in respiratory alkalosis, pCO2 decreases
88
What happens in acute, life-threatening status asthmaticus?
The patient becomes unable to ventilate properly, and pCO2 increases vastly, causing respiratory acidosis
89
What happens in hyperventilation?
There is increased expiration of CO2, resulting in reduced pCO2 and respiratory alkalosis. This is also similar to how mild asthma attacks occur, as the patient experiences an increase in ventilatory drive without respiratory failure
90
What is metabolic acidosis and what can cause it?
Decreased availability of bicarbonate (likely due to increased acid production that exceeds renal excretion). The bicarbonate is used up as a buffer, and the acid concentration builds.
Can be caused by increased acid production in terms of lactic acidosis (due to poor tissue perfusion), or diabetic ketoacidosis.
May be due to decreased acid excretion, in terms of renal failure and renal tubular acidosis
Can be due to bicarbonate loss, such as in severe diarrhoea or ileostomy
91
What is metabolic alkalosis?
Increased availability or production of HCO3- and subsequent decrease in acid concentration. Often due to loss of acid due to vomiting, extra ingestion of sodium bicarbonate etc. When the equation shifts towards the acid side, the unlimited CO2 and H2O can form more HCO3-
92
What are the hallmarks of each alkalosis/acidosis condition?
Metabolic alkalosis has high pH, high bicarbonate and normal pCO2
Respiratory alkalosis has high pH, normal bicarbonate and low pCO2
Metabolic acidosis has low pH, low bicarbonate and regular (early) or low (late) pCO2
Respiratory acidosis has low pH, regular bicarbonate and high PCO2
93
What is respiratory compensation in metabolic acidosis?
Low pH stimulates ventilation, causing a drop in pCO2. This partially returns pH to a more normal value
94
What role do the kidneys play in acid-base balance?
They produce new bicarbonate, they excrete NH4+ and TA acid, and allow bicarbonate to be reabsorbed
This is called net acid excretion- amount of NH4+ excreted, amount of TA excreted, minus the HCO3- excreted x the volume
95
How are the kidneys involved with HCO3-?
They reabsorb it along with Na+, using carbonic anhydrase to convert it to CO2 and H2O, before taking it in and using the same enzyme to change it back
96
How is H+ secreted in the distal tubule and collecting duct?
It may be attached to NH3 formed from glutamine, although most NH3 is reabsorbed in the TAL In the collecting duct, diffusion trapping places H+ on free NH3, allowing it to be secreted.
97
How does the kidney respond to acidosis?
It increases HCO3- and H+ transport along the nephron
It increases its availability of urinary buffers as well as increasing ammoniagenesis.
This causes generation of bicarbonate, so even though CO2 might have increased in respiratory acidosis, the HCO3- becings to increase, pulling the pH back to a more reasonable level
98
What is a clinical example of renal compensation?
Eg. A 60 year old who has been smoking for 40 years- has a normpal but low pH, a high pCO2, high bicarbonate.
99
What happens to renin secretion in each kidney if one artery becomes obstructed?
In the obstructed kidney, flow rate decreases and so does perfusion pressure, triggering the release of renin. This goes on to cause increased angiotensin II, causing an increased in systemic blood pressure. Because of this, the left kidney decreases its production of renin
100
What can trigger the release of aldosterone?
Increased levels of angiotenin II and increased K+
101
How does aldosterone act in the body?
It binds to mineralocorticoid receptors and increases the production of ENaC channels to be inserted into the luminal side of the principal cells, absorbing more Na+ and water into the blood
102
What can occur due to hyperaldosteronism?
High blood pressure due to increased retention of salt and water
103
What happens if the function of aldosterone is 100% lost?
Other reflexes to Na+ deficiency can be used, such as a reduction in GFR
104
What can cause increased vs. decreased Na+ reabsorption?
Increased: RAA system, SNS activity, ADH
Decreased: ANP, decreased RAA and SNS, dopamine and prostaglandins
105
What is ANP?
Produced by atria due to increased filling pressure and stretch. It decreases Na+ reabsorption in the distal tubule and outer medullary collecting duct by blocking ENaC channels
It also inhibits the release of aldosterone and renin, and vasodilates the afferent arteriole to increase GFR
106
What are the processes that occur when the body gets dehydrated?
Increased osmolarity leads to osmotic receptors sensing it and causing release of ADH, which acts on the V2 receptor to cause increased H2O retention
Decreased blood volume triggers ANP
Decreased blood pressure triggers baroreceptors to increase SNS activity
107
What is the main result of kidney failure and what are its two subtypes?
Low GFR
| Subtypes are acute kidney injury, and chronic kidney disease
108
What are the blood tests that can indicate kidney failure?
- Urea in blood
| - Creatinine in the blood- if the kidney can't excrete it the levels will rise.
109
What extra-renal factors will affect plasma creatinine?
Age- older people have decreased muscle mass and so less creatinine
Weight- more muscle mass means more creatinine
Gender- men have higher muscle mass
110
What is eGFR?
Estimated glomerular filtration rate- it accounts for creatinine as well as age and sex, taking into account muscle mass- however, it only works for patients with stable creatinine, as well as not working for those with unusual muscle mass- eg. amputees.
111
What is acute kidney injury and what can be its categories of cause?
```
- It's a sudden and rapid reduction in GFR that is usually reversible. It's mostly due to non-renal causes
Injury can be:
- Pre renal
- Renal
- Post Renal
```
112
What can cause pre-renal kidney failure?
Low blood pressure (as blood is redirected to more essential organs) or not enough blood to the kidneys, due to dehydration, septic shock, haemorrhage, cardiogenic shock or severe renal artery stenosis
113
What are the examination symptoms of the different causes of pre-renal kidney failure?
Low BP- postural drop
Dehydration- Low JVP, decreased tissue turgour
Sepsis- fever
Haemorrhage- bleeding
Signs of cardiogenic shock- heart failure/pulmonary oedema
Low initial urine output
114
What do test and treatments find in pre-renal failure? What are possible consequences?
A high creatinite in the blood, as well as hyperkalaemia, high phosphate and potentially low calcium
Treat the underlying problem, such as rehydrating, antibiotics, treatment of haemorrhage, or ICU admission for consistent low BP
If it doesn't get better, it can go on to acute tubular necrosis
115
What is acute tubular necrosis?
Consequence of untreated pre-renal kidney failure.
Needs to be treated by maintaining a norma BP and treating the underlying condition. If the kidneys get worse, dialysis can keep the kidneys alive while they heal, but is not a treatment in itself
Most get better
May show a polyuric phase- tubules aren't able to concentrate the urine, so up to 20L a day may be produced
116
What is glomerulonephritis?
One of the causes of renal kidney failure (besides ATN)- due to inflammation of the glomerulus. It's the main cause of acute kidney injury, due to vasculitis or infection
It presents with blood and or protein in the urine, and is diagnoses with renal biopsy
117
What are some post renal causes of kidney failure?
Due to blockage or squashing of post-renal structures. It can be due to kidney stones, tumour, prostate hypertrophy or urinary retention.
118
What is Chronic Kidney Disease and what can cause it?
It's a gradual decline in renal function that is irreversible. It presents with elevated creatinine and urea, although urine output is normally usual.
It can be caused by diabetes, glomerulonephritis, and hypertension, among others
119
What are the symptoms of those with chronic kidney disease?
Usually none in the early stages, and are found on blood tests. Can sometimes have uraemia if the case is severe enough. Most common sign is hypertension, with oedema, pulmonary oedema and a raised JVP
120
What is uraemia?
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Anorexia
Nausea
Vomiting
Itchiness
SOB
Cold intolerance
Swelling
Seizures
Coma
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121
Why does chronic kidney disease present with anaemia?
The kidney makes erythropoietin, which makes the bone marrow produce RBCs. Kidneys in failure will not produce this correctly. However, this does not present for a while as RBCs have a life of about 3 months
122
How does chronic kidney disease present with bone disease?
The kidneys produce 1-hydroxylase, which transforms vitamin D into a useable form to allow Ca2+ and P to be used.
Phosephate is excreted less, there is a low vitamin D and a low calcium. there is also a high parathyroid stimulation due to low Ca2+ and high K+, resulting in excessive calcium resorption in the bones, fractures, extra-osseous calcification and vascular calcification (causing thrombosis and embolism)
123
What is concerning about high potassium in CKD?
The kidneys don't excrete K+, causing arrhythmias. This can increase mortality
124
How is CKD treated?
Mainly by preventing failure from growing worse, and controlling its implications
125
What are the stages of CKD?
1- GFR slightly reduced
2. GFR reduced, increased PTH
3. GFR much reduced, decreased Ca2+
4. GFR borderline, has anaemia, CV risk, high P, acidosis and hyperkalaemia
5. GFR less that 15ml/min, presents with uraemia
126
What are the clinical presentation and problems that can be due to generalised parenchymal disease?
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Haematuria
Proteinuria
Acute nephritic syndrome
Nephrotic syndrome
CKD
Need to assess renal function
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127
What are the clinical presentation and problems that can be due to collecting system abnormalities?
Present with infection, polyuria, renal colic and CKD
| Assess renal function
128
What are the clinical presentation and problems that can be due to Focal lesions?
Haematuria
Backache
Need to exclude malignancy
129
What is the scale of glomerular filter function?
Can range from blocked glomerulus (decreased GFR) to leaky (much increased GFR)
130
What is proteinuria and what causes it?
Normally, the glomerulus filters proteins and the tubules reabsorb them. However, larger proteins are not able to pass through, and those that are are reabsorbed
If the filter is leaky, larger blood constituents can leak through the glomerulus.
Proteinuria involves mainly albumin and small amounts of others. It ca be measured with a 24h urine test, looking at ratios of albumin to creatinine and protein to creatinine.
131
What is microabuminuria?
30-300mg in 24h.
| It can be caused by diabetes, fever, exercise, heart failure or poor glycaemic control
132
What is nephrotic syndrome?
More than 3.5 g urinary protein per day. Low serum albumin and oedema
Frothy urine, hypercholesterolaemia, blood clots and normal or impaired renal function
Reduced metabolism leads to increased triglycerides
Low oncotic pressure leads to lipoprotein production in the liver, triggering increased cholesterol production
Malnutrition
Risk of thromboembolism
Reduction in antibody production can increase bacterial infection
133
How does kidney failure cause oedema?
Increased excretion of large proteins like albumin means the liver can't keep up and oncotic pressure decreases, reducing fluid reabsorption in the capillaries (due to starling's law of ultrafiltration). This can also decrease plasma volume and cardiac output, triggering the RAA and more to retain Na+ and H2O
134
How does controlling BP help to control proteinuria?
An increased BP pushes more proteins through the glomerulus.
135
How can acute glomerulonephritis cause proteinuria?
Can cause leaky glomeruli as well as nephritic syndrome
136
What is the difference between nephrotic and nephritic syndromes?
Nephritic syndrome involves inflammation in the glomerulus and involves oliguria, hypertension, volume overload, haemoptysis, rash, arthritis and fever as well as red cell casts- glomerulus is so damaged that it lest through damaged RBCs
Nephrotic syndrome is oedema, proteinuria, hypoalbuminaemia and hyperlipidaemia
137
How do you treat proteinuria?
Find the cause, generally with a biopsy. Manage blood pressure
138
What is haematuira?
Microscopic or macroscopic amounts of blood in the urine
139
What causes haematuria?
Bleeding from somewhere in the urinary tract, due to glomerular, collecting system injuries or focal lesions.
140
How does collecting system haematuria present?
Usually macroscopic with little to no proteinuria
| Can be due to kidney stoles etc.
141
How does focal lesion haematuria present?
Macro or microscopic
Often asymptomatic, with back ache and mass.
Can be renal cell carcinoma in the tubules, which make up 90% of renal cancer. Due to smoking or genetic factors mainly
Macroscopic masses are well circumscribed, mottled red, yellow and brown, and spread if they invade the renal veins
142
How do renal cell carcinomas present?
Symptoms occur late with haematuria and potential clots.
Flank pain, abdominal mass, and ectopic hormone production are also side effects
Local spread isn't common, and survival is less than 50%
143
What is the best approach to interpreting acid-base data?
1. Decide primary diagnosis- acidaemia/alkalaemia, and then acidosis or alkalosis. Is the primary disturbance respiratory or metabolic?
2. Is the compensation appropriate? If not, there's more than 1 disorder
3. Calculate the anion gap- high anion gap means metabolic acidosis
4. Calculate the dAG/dHCO3- ratio: helps to identifying a coexisting metabolic alkalosis or acidosis
Can use an acid base map- if between conditions, then different pathologies are combined.
144
What are the primary changes and compensatory responses for each of the acid-base disorders?
Metabolic acidosis is decreased HCO3-, with decreased pCO2 to compensate
Metabolic alkalosis is increased HCO3-, with increased pCO2 to compensate
Resp. disorders can be acute or chronic due to kidneys taking time to compensate
Acute resp. acidosis is increased pCO2 with a small amount of increased HCO3-, whereas chronic shows a larger HCO3- increase
Acute resp. alkalosis is decreased PCO2 with a small amount of decreased HCO3-, while chronic shows larger reductions in HCO3-.
145
What is base excess and what does it mean?
Base excess is the amount of acid or base needed to restore pH to 7.4. It's calculated from pH, pCO2 and haemoglobin. Normally base excess is 0, with a range from -2 to 2. It is positive in metabolic alkalosis and negative in metabolic acidosis
146
Describe the pattern seen in post-hypercapnic alkalosis
On admission, chronic lung disease will give respiratory acidosis with renal compensation. When ventilation is started, the pCO2 decreases, but the kidneys continue to produce increased HCO3- to compensate, resulting in metabolic alkalosis
147
What is the anion gap and what can it be used for?
Anion gap is (Na + K) minus (Cl + HCO3-). Normally, it ranges between 14-18 due to negatively charged protein anions. An increased AG indicates the presence of unmeasured anions like lactate. This can be due to the addition of HCO3- and -ve protein buffers to buffer the acid, as well as an increase in unconjugated anions.
148
How do we respond to suspected metabolic acidosis and what can cause it?
Firstly we confirm that it is low pH with low HCO3-. We check the anion gap, and if it's high it's acid gap acidosis (and if not, it's non anion gap acidosis). If there's a normal serum AG we can check urine AG
We can also check the change ratio to see if the disorder is mixed
Causes are KULT- Ketoacidosis, uraemia, lactic acidosis and toxins
149
What is the dAG/dHCO3- ratio?
If it is between 1-2, then there is a pure anion gap acidosis
If the ratio is below 1, then we have a greater loss of HCO3- per AG change- a concurrent normal anion gap acidosis
If over 2, there is a concurrent metabolic alkalosis as we have a larger AG change to lose the same amount of HCO3- ions
150
Describe normal anion gap acidoses
Most commonly a non-renal cause, like diarrhoea, ileostomy or loss of pancreatic and biliary secretions.
They can also be due to renal causes, like PCT acidosis, hypo or hyperkalemic distal renal tubular acidosis, and chronic kidney disease
Renal tubular acidoses are defects in acid excretion, so that urine pH is greater than 5.5 and shows no increase in ammonium.
Hyperkalemic DCT acidoses are often due to aldosterone deficiency or resistance
151
Describe the presentation of a child with rickets, and why this anomaly is observed
The child will present with high Cl content and a low base excess, although show no serum anion gap due to to the high Cl concentration Upon test of a urine anion gap, we can see that pH is high and ammonium is low, so the UAG is positive, showing low NH4+.
The increase in Cl is due to extra Cl being resorbed to maintain electroneutrality with Na+ reabsorption, as bicarbonate is so low.
152
How does potassium relate to acid base?
H+ and K+ tend to exchange themselves when moving in and out of cells to maintain electroneutrality. When there is an acidosis, it may be causing (primary) or caused by (secondary) hyperkalaemia, and vice versa.
The two ions also compete with each other for secretion, so when there is acidosis, more H+ is excreted at the expense of K+, and vice versa. The most important exceptions are diarrhoea due to K+ being lost as well as bicarbonate, and RTA, where the distal and proximal tubes are also assoc with hypokalemia
153
How does vomiting causes alkalosis?
HCL is lost from the stomach, and hypokalemia results from both the alkalosis and K+ loss. They hypokalemia causes muscle weakness.
154
Describe metabolic alkaloses and their responsiveness to Cl-
Chloride responsive alkaloses are due to vomiting or gastric damage (due to loss of HCl) and diuretic induced alkalosis (due to K+ and Cl- loss)
Chloride resistant alkaloses are due to mineralocorticoid excess like aldosteronism, severe hypokalemia and antacid ingestion
155
Describe chloride responsive alkalosis
In a metabolic alkalosis the kidney attempts to increase HCO3- loss, and if Cl is depleted, reabsorption of HCO3- becomes necessary to oreserve sodium balance. This means the kidney cannot correct the alkalosis.
156
What is the difference between arterial and venous blood gasses?
In patients with reasonable perfusion, pH, HCO3- and BE are almost identical between the two. Only do arterial puncture when pO2 is needed or there is circualtory failure
157
What are some artefacts that can be found in taking blood gasses?
Air in the syringe can give falsely low pCO2 and an apparent resp. alkalosis
Delayed separation of the plasma from RBCs can enable them to produce lactic acid, which gives a metabolic acidosis with a high AG
158
What are the main ligaments of the pelvis?
The inguinal ligament- stretches from ASIS to pubic tubercle, formed from edge of Ext. oblique aponeurosis
The lacunar ligament- connects the ingunal and pectineal ligaments
The pecineal ligament- runs along the pecineal line of the bubic bone. It's incredibly strong and a good place to anchor sutures into.
159
Describe the inguinal canal (males and females)
It's an oblique passage through the lower abdominal wall. It extends from deep to superficial inguinal rings.
In males, it carries structures to and from the testis and abdomen via the spermatic cord, and holds the ilioinguinal nerve
In females, it carries the round ligament of the uterus from the pelvis to the labia majora, and the ilioinguinal nerve.
160
Describe the deep inguinal ring
An opening in the transversalis fascia, halfway between the ASIS and in the pubic symphysis- the mid-inguinal It's just above the inguinal ligament and lateral to the inferior epigastric artery.
In the spermatic cord it gives rise to the internal spermatic fascia, and the fascia of the round ligament in women.
161
Describe the superficial inguinal ring
A triangular shaped defect in the aponeurosis of the external oblique, superolateral to the pubic tubercle. Its margins give rise to the external spermatic fascia. It has two crus, or legs, in the defect- lateral and medial
162
Describe how the TA and int. ob give rise to the inguinal canal
The transversus abdominis does not contribute to the spermatic fascia
The internal oblique gives rise to the cremasteric muscle of the spermatic cord
Both come together to form the conjoint tendon on the pectineal line
163
Describe the borders of the inguinal canal
Anterior wall is the aponeurosis of the external oblique, and the internal oblique in the lateral 1/3 of the cord
Floor is formed by the inguinal and lacunar ligaments (lacunar only medial)
Roof is formed by fibres of the Transversus abdominis and int. ob.
Posterior wall is formed by trans. fascia and conjoint tendon
164
What is hesselbach's triangle?
It's often the site of a direct hernia, and corresponds to a weak anterior wall, just medial to the sup. ing. ring
Its medial border is the lateral rectus abdominis muscle, lateral is the inferior epigastric artery, and inferior is the inguinal ligament
165
Describe the spermatic cord and its layers
It's a collection of structures that passes along the male inguinal canal and into the testis. It begins at the deep inguinal ring and ends at the testis
It arises from a peritoneal diverticulum (pouch) called the processus vaginalis
The transversalis fascia forms the internal spermatic fascia, the int. ob. gives the cremaster muscle, and the ext. ob. gives the ext. spermatic fascia. The peritoneal outpouching eventually pinches off, leaving a closed off sac called the tunical vaginalis as a remnant
166
How do layers of fascia change when they reach the scrotum?
The scarpa's and camper's fascias fuse and become the dartos- continual posteriorly with the deep perineal fascia called colles fascia. It also receives blood from the internal and external pudendal arteries
167
What are the contents of the spermatic cord?
3 Arteries: Testicular from L2 aorta, artery of vas deferens, and cremasteric artery
3 Nerves: The genital branch of genitofemoral (innervate cremaster and skin of scrotum) , the sympathetic nerves from the testicular plexus, and the ilioinguinal (although this travels just outside the cord)
3 Other structures: The vas deferens, lymphatics (drain to para-aortic nodes) and tunica vaginalis
The pampiniform venous plexus- helps with temp control
168
Describe testicular torsion and how to diagnose it
Testicular torsion is a surgical emergency due to twisting of the spermatic cord, cutting off blood and causing ischaemia. It presents as acute and severe testicular pain, also sometimes referred to the groin. Nausea and vomiting
In normal males, the cremasteric reflex is observable when the skin of the upper medial thigh is stroked, and the testicle is drawn up (due to stimulation of femoral branch and ilioinguinal nerves). This stimulates the genital branch, causig the cremaster to contract
In testicular torsion, this reflex is not present.
169
Describe direct vs. indirect hernias as well as femoral vs. inguinal hernias
Femoral hernias occur inferior to the inguinal ligament and are more common for females. The loop of bowel pushes through the femoral canal, and can be released by cutting the lacunar ligament
Inguinal hernias pass superior to the inguinal ligament and are more common in males.
These can be subdivided into direct and indirect inguinal hernias
Direct hernias push through a weakness in the posterior wall of the inguinal canal- Hesselbach's triangle. They don't pass through the deep inguinal ring, move medial to the epigastric artery and are more common in older patients.
Indirect hernias pass through the inguinal canal and into the spermatic cord. They pass through the deep inguinal ring, are lateral to the inferior epigastric artery, and are more common in the juveniles
170
What are the bones of the sacrum?
The ala are the 'wings'
In the centre is the sacral canal
Sacral bodies and anterior and posterior foramen are fused
The cornu at the bottom of the canal is just inferior to the sacral hiatus, and the coccyx is at the very tail
171
What forms the boundary between the true and false pelvis?
The true pelvis is below this line, the false pelvis above it
The boundary is formed by the ring of the sacrap promontory, ala of the sacrum, arcuate line, pectineal line, pubic tuburcles, crest and symphysis.
172
What is pelvic tilt and how do male and female pelvises differ?
Pelvic tilt describes how the ASIS is actually vertically aligned with the pubic tubercle, rather than sitting like a bowl. All boundaries except the floor of the pelvis are of bone (floor is pelvic floor muscles)
Male pelvises have higher, narrower ilia, a heart shaped inlet and outlet (as opposed to round) and have the ilia closer together
173
What are the ligaments forming the foraminae of the pelvis?
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The sacrotuberous (from sacrum to ischial tuberosity) and sacrospinous (from sacrum to ischial spine)
The sacrum is also joined to the ilia by the anterior and posterior sacroiliac ligaments
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174
What are the two pelvic wall muscles and what foramen are they associated with?
Piriformis runs through the greater sciatic foramen from the anterior sacrum to the greater trochanter
Obt. internus fills the lesser sciatic foramen
175
Where do the pelvic vessels run?
Above piriformis is the superior gluteal vessels and sup gluteal nerve
Below piriformis is the inf. gluteal vessels and nerve, sciatic nerve, post. fem. cutaneous nerve, and the internal pudendal vessels and pudendal nerve run through the greater foramen and hook around the ischial spine before reentering the lesser sciatic foramen.
In the obturator canal is the obturator nerve and vessels
176
What are the branches of the anterior division of the internal iliac artery?
3 vesicular: Umbilical artery (though fibrous after birth), superior vesical arteries, either 2 or 3, and inferior vesical artery
3 visceral: Obturator artery, internal pudendal and inferior gluteal artery
3 parietal: Middle rectal, urterine (f) and vaginal/prostatic artery
177
How does the anterior division of the internal iliac artery differ between male and female?
Males' inferior vesical and middle rectal supply the prostate, seminal vesicles and ductus deferens.
The testicular arteries come off from aorta L2
Females' uterine artery gives off the vaginal artery
The ovarian arteries branch from aorta L2
178
What are the branches of the posterior division of the internal iliac artery?
Iliolumbar artery supplies post. abdominal wall muscles
Lateral sacral pushes through the sacral foramina to supply the sacral canal
Continues on to give the superior gluteal artery
179
Describe the venous drainage of the pelvis
Venous plexuses surround the bladder, prostate, rectum, uterus and vagina, draining via the internal pudendal veins to the internal iliac veins
180
What is the sacral plexus? Describe the nerves coming from it
The sacral plexus is found on the surface of piriformis, and comes from S1-4 from the anterior sacral foramina.
The superior gluteal nerve is L4-S1, and goes to gluteus med and min
The inferior gluteus is L5-S2 and goes to glut max. These pass sup. and inf. to piriformis, respectively
The sciatic nerve is L4-S3, with the dibial leaving below piriformis
Levator ani is from S3-4. It is at risk of compression as it sits on the pelvic floor
The pudendal nerve is S2-4 and branches into inf. recatal, perineal, dorsal to clitoris/penis, and scrotal/labial nerve
181
Describe the autonomic nervous supply of the pelvis
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The superior hypogastric plexus from ant. L5 and sacral promontory, and the inferior hypogastric plexus from the pelvic floor provide symp. supply from L1-2 for continence, ejaculation, and movement along epididymis
The parasympathetic (s2-4 causes vasodilation for erection and contraction of the bladder
Agitation of the pelvic viscera can cause nausea, as the abdominal and pelvic nerves are interlinked
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182
What syndromes are we looking for in antenatal renal imaging?
Agenesis (presents with no amniotic fluid and no kidneys
Polycystic kidneys (one or both kidneys affected)
Reflux (MCU)
183
Describe MCU
Micturating cystourethrogram
Normally the ureters enter the bladder at a 45 degree angle so that they are able to be clamped off when the bladder swells. If they enter vertically there is no clamping and the more full the bladder gets the more urine is pushed back up into the system- presents with largely dilated ureters
184
Describe posterior urethral valves
A small blockage between the tube connecting the bladder and the urethra- the post urethral valves cause little flow of urine to come from the bladder- can feel bloating, and in baby boys pee is a dribble, not a stream
185
Diagnose & describe how to image: 25yo, loin to groin pain, afebrile, normal W
Kidney stones
Start with CT at low dose with plenty of pain relief, as most renal colic patients have difficulty lying still.
Stones show perinephric, periureteric stranding and hydronephrosis
Stones greater than 6mm are unlikely to move by themselves and often need surgical intervention
186
Diagnose and describe how to image: 42yo woman, right flank pain, febrile, high WCC
Infection.
| Use ultrasound and then low dose CT to look for areas of pus and swelling
187
Diagnose and describe how to image: 85yo main with recurrent UTIs
Likely obstruction due to BPH.
| Can look for dilated renal pelvises using ultrasound followed by size of prostate
188
Diagnose and describe how to image: 22yo decreased renal function
Ask fHx
| Start with ultrasound- likely cysts, due to adult polycystic kidney
189
Diagnose and describe how to image: 25yo crashed mountain bike
Find out of blood in urine
Give a CT, look for tamponade in the retroperitoneum
Give dye to see whether a kidney is still being perfused
190
Describe how the uterus presents on imaging
It's a whiteish pear shaped organ, behind the bladder. It is pushed backwards by a full bladder and moves forward when it's empty/ Behind the uterus is the pouch of douglas
Oocytes are released into the abdominal cavity before being taken up by fimbriae, so infection there can cause ectopic pregnancy etc.
191
How does the endometrium change during a cycle?
Normally imaged as a white line as both sides are pressed together. During ovulation it develops a sort of halo
192
Describe pathologies observable in imaging the female reproductive organs
Fluid in the pouch of douglas may be a ruptured oocyte or menstruation (normal)
It can also mean inflammation or ectopic pregnancy
Many developed but not dominant eggs can sit in the ovary and not be ovulated- results in polycystic ovarian syndrome
Fluid above and below the ovary can be due to cancer, causing ascites
Dye injected into the uterus travels along the fallopian tubes. If not spilled into the abdomen, likely a blocked fallopian tube
Loss of pelvic floor also shows bladder sliding into base of pelvis during standing
193
How do infections spread in the male testis?
Often start in the tail of the epididymis, and move into the testicle
194
How does testicular torsion present on ultrasound?
Abnormal blood flow to one testis
195
How does epidiymitis present on ultrasound, and how does this compare to the presentation of a tumor?
Inflammation is normally due to STDs, or else strep. or e. coli in children. Presents as a swollen epididymis and huge blood flow
Testicular tumors present as lumps in the testis, as well as presenting with lung cancer
196
How do we image the prostate?
Increasingly with MRI, but can also do trans abdominal and trans recta ultrasound
MRIs show us tumor localisation as well as its spectroscopy
197
Describe the borders of the pelvic outlet
It is shaped like a diamond- the pubic symphysis is at the anterior aspect, with the ischiopubic ramus and ischial tuberosities going down the diagonal sides, the sacrotuberous ligaments making up the posterior sides, and the coccyx making the posterior apex
198
Describe the triangles within the perineum
Anteriorly is the urogenital triangle, which contains the genitals and the urethra
The anal triangle forms the posterior triangle (also angled posteriorly), which contains the anal orifice
199
Describe the perineal body
It's a mass of fibrous connective tissues that forms the site of many muscle attachments. It lies in between the anal and urogenital triangles
Attaching to the perineal body are the levator ani, bulbospongiosus, external anal sphincter and perineal muscles
200
Describe the muscles making up the pelvic floor
Two main muscles- levator and coccygeus.
Levator ani can be divided into iliococcygeus, ischiococcygeus and pubococcygeus. It is innervated by the pudendal nerve (S2-4) from below, and the nerve to levator ani (S3,4) from above
Iliococcygeus attaches to the fascia of obturator internus and prevents prolapse of the pelvic viscera. It may be damaged by childbirth
Pubococcygeus can be divided into more groupings, the most important of which is puborectalis. This muscle forms a sling around the rectum to angle it and maintain continence. A loss of the nerves to the pelvic floor can therefore result in incontinence.
201
Describe the muscles of the external anal sphincter
It is formed from skeletal muscle, running from the perineal body to the anococcygeal ligament. It causes anal closure, and is supplied by the pudendal nerve (S2-4)
202
Describe the muscles of the internal anal sphincter
Smooth muscle deep to the external anal sphincter, and separated from them by connective tissue
203
Describe the ischioannal fossa
They are mainly fat filled structures that allow for expansion and contraction during defecation.
They exist between the ischial tuberosities laterally, the coccyx posteriorly, and the perineal body in their anterior midline. It is best to avoid their lateral apices during surgery as this is where the pudendal structures enter and leave
204
Describe the anal canal
The internal anal sphincter runs closest to the border of the anal canal, with puborectalis more superficial and superior and the external anal sphincter running inferiorly from its attachment to this muscle. Within the rectum are the anal columns, which contain some vessels.
Above the transition from rectum to anal canal, the tissue is supplied by the ANS, and is lined with a mucous membrane. Below, the canal is lined with skin and supplied by the SNS
205
Describe the supply and drainage of the anal canal
Superiorly, it's supplied by the IMA and drained by the superior rectal vein to the IMV. Its nodes drain to preaortic nodes at L3
In the midline, it's supplied by the middle rectal artery from the internal iliac, and lymph goes to internal iliac nodes
Inferiorly, it's supplied by the inferior rectal artery from the internal pudendal artery, and lymph goes to the internal iliac nodes.
At the border between the rectum and anal canal, venous drainage transitions from portal to systemic. This means that anal varices are able to form due to portal hypertension
206
Describe haemorrhoids
These are inflamed venous plexuses that can form in the internal or external anal canal- external are more painful as they're supplied by somatic nerves
207
Describe the perineal membrane
A horizontally running membrane that stretches across the urogenital triangle to prevent organ prolapse. It forms an attachment site for muscles, with a defect anteriorly for the passage of the deep dorsal veins of penis/clitoris, and a urethral (and vaginal) hiatus. It covers up the anterior deficiency in the pelvic floor muscles
208
Describe the basic structure of the deep perineal pouch
Superior layer of fascia blended with perineal body and membrane, with muscle attachments underneath and a final layer of fascia that forms the perineal membrane
209
What is contained within the deep perineal pouch, and how does this differ between sexes?
It contains the deep transverse perineal muscles and the external urethral sphincter
In men, it contains the membranous urethra, bulbourethral glands, and neurovascular tissues
In women, it contains the vagina, the compressor urethrae and urethrovaginalis muscle, as well as the dorsal nerve of the clitoris
There are more muscles in the female deep perineal pouch as their urethra is much more direct and less convoluted, meaning they need more structures to help maintain continence
210
What is contained within the superficial perineal pouch?
These are the structures between the perineal membrane and the skin
It contains nerves and vessels, erectile tissues, perineal muscles, and bartholi's glands in females
211
Describe the pathways of the fascias of the body
Scarpa's fascia becomes continuous with the dartos fascia within the penis and scrotum, which also becomes continuous with the colles fascia in the perineum.
In trauma, this means that bleeding can move into the abdomen even if it is from the perineum
212
Describe the course of the internal pudendal artery and some of its main branches
It comes from the internal iliac, branches into the sup. gluteal (umbilical) and then gives off the inf. gluteal before continuing on as the internal pudendal artery
It branches into inferior rectal, perineal, and dorsal artery of the penis/clitoris
The nerve comes from S2-4, and supplies the perineal muscles, external urethral sphincter, and skin of the genitalia and perineum as well as the erectile muscles
213
How does defecation and micturition come about in terms of muscle relaxation?
To defecate, we relax puborectalis using the pudendal n and n to levator ani
We relax the internal and external anal sphincters, using the paraxymphathetic plexus (S2-4) and pudendal nerves respectively
Rectal muscles are then relaxed with the pelvic parasympathetic nerves, to cause a wave of contraction
We also increase intraabdominal pressure with the SNS, causing diaphragmatic and abdominal constriction as well as closure of the larynx
To micturate, our response is by voluntarily relaxing he external urethral sphincter with the pudendal nerve, and contracting the detrusor muscle with the parasympathetic splanchnic nerve
In children, this is a sacral reflex, where filling the bladder activates afferent and efferent ANS signals to initiate micturition- this does not transfer to CNS control until later
214
Which area of the perineum is not useful for assessing pudendal nerve function?
The anus- as this is supplied by dermatome S5, which is not part of the pudendal nerve (S2-4)
215
What pouches are present within the male and female genitalia?
Vesicorectal pouch in the male lies between the bladder and the rectum
In the female, there is the vesicouterine pouch, but the important one is the rectouterine pouch (pouch of douglas).
216
Describe the muscles within the perineum
In both males and females, there is ischiocavernosus, which is attached along the ischiopubic rami and aids erections in males and tenses the vagina in females
There is also the bulbospongiosus muscle, which is attached posteriorly to the perineal body
217
How do perineal muscles differ between males and females?
Males' bulbospongiosus muscles are attached in the midline, while females' are split either side of the vaginal orifice. Additionally, the function of this muscle in males is to aid erection and ejaculation, while in females it is associated with clitoral erection and feelings of orgasm
218
Describe the erectile tissues of the male and female
Females: The crus of the clitoris contribute to the body, while the bulb of the vestibule contributes to the head
In males, the crus of the penis becomes the corpus cavernosum as it leaves the body, while the bulb of the penis becomes the corpus spongiosum and glans penis, which contain the urethra
219
Describe the vasculature of the penis
All are branches of the internal pudendal artery and vein
There are two dorsal arteries that accompany the dorsal nerve of the penis. These are below the deep fascia of the penis, running with 1 deep dorsal vein passing through the anterior deficiency in the perineal membrane
There are two deep arteries inside the corpus cavernosum, as well as two superficial dorsal veins of the penis between the superficial and deep fasciae
The female structures are equivalent, but much smalelr
220
What are the functions of the testes and what is their anatomy?
They create sperm, and are surrounded by a fibrous capsule
They are separated into lobules, each with 1-3 seminiferous tubules which open into the rete testis. The efferent ductules connect the rete testis to the epididymis, which stores sperm before becomming the vas deferens
221
Where does the vas deferens run within the body?
It travels through the inguinal canal inside the spermatic cord, joining the duct from the seminal vesicles to form the ejaculatory duct. This then runs into the prostate to enter the urethra
As it enters the body it enters lateral to the inferior epigastric artery, and crosses over the external iliac vessels passing medially into the prostate. It passes over the ureter to join the seminal vesicles, so can be remembered as having 'water under the bridge'
222
Describe the seminal vesicles
They are coiled organs on the posterior side of the bladder that secrete the liquid component of semen as well as fructose. They lie superior to the prostate
223
Describe the prostate, and how this can change in pathology
It is a gland inferior to the bladder which produces alkaline fluid rich in enzymes and phosphatase
It contains the prostatic urethra and ejaculatory duct, supplied by braches of the internal iliac artery and is drained by the deep dorsal plexus to the internal iliac vein.
If it gets enlarged it can be benign or malignant, and can affect all or part of the prostate. This can contrict the uretra, cause resevoirs of urine (unable to void fully) and may extend up into the bladder (issues with continence as the ring can't close
224
Describe the overall pattern of lymphatic drainage in the male genitals
Most drain to iliac nodes, but the testicles drain to para-aortic nodes and the skin drains to the inguinal nodes
225
Describe the organisation of the uterus, and its angles
The cervix is joined to the vagina at the fornices, before moving into the body and fundus (top). The fallopian tubes contain the isthmus, then the ampulla, and finally the infundibulum with the fimbriae
In 50% of women the uterus is anteverted, where the angle of antiversion runs between the vaginal trajectory and then curves over as the uterus projects anteriorly. The angle of anteflexion is between this projection of the uterus and its curvature over the bladder.
226
Describe the ligaments of the uterus
The broad ligament is a subdivision of the peritoneum like a mesentery, where it wraps over the uterine tubes and surrounds the uterus.
The uterine artery runs within it overtop of the ureter
The mesovarium connects the ovary and fallopian tubes, the suspensory ligament of the ovary connects ovary to pelvis, and the ligament of the ovary connects the ovary to the uterus
227
Describe the blood supply of the ovary
It's supplied by the ovarian artery from L2 aorta, and drained by the ovarian vein (on the RHS this runs to the IVC, and on the left it goes into the L renal vein first)
It is supplied by the ovarian nerve plexus
228
Describe the vestibule
It is a structure of external female genitalia, which is englosed by the labia minora. It includes the urethral opening, clitoris, vaginal opening and bartholi's glands
229
Describe the general lymphatic drainage of the external female genitals
Most goes to the iliac nodes, but ovaries go to L2 para aortic nodes and skin structures go inguinal
230
Describe bartholin's glands and how this can develop pathologically
They are glands responsible for mucus secretion, sitting posterolaterally to the vaginal opening. They are found in the superficial perineal pouch
If they get blocked they can form a cyst, which if exposed to bacteria may form an abcess and cause infection.
231
Describe the consequences of a 5-a-reductase deficiency
Testosterone is not converted to DHT, meaning a male is born with female primary genitalia. As they hit puberty, they get a surge in the stronger version of the androgen, causing the development of male genitalia later in life
232
Describe how a patient with AKI may present. How do we distinguish whether she is AKI or CKD?
Afebrile, low BP, dry skin, clear chest and JVP of 0cm- patient is intravascularly dry and dehydrated
Bloods show elevated urea and Cr, and reduced GFR
Ca will be low and P will be high
Most useful distinction is done by looking a Hb- AKI will have normal Hb as RBCs have a long half life
233
How do you distinguish whether an AKI is pre-, post- or renal?
Most likely to be pre-renal due to decreased kidney perfusion. These patients generally have a low BP due to bleeding, sepsis, dehydration or HF, and it may progress to intrinsic renal damage
Renal is mainly due to ATN, due to untreated pre-renal issues or nephrotoxins (commonly NSAIDs and contrast
RPGN is typically due to SLE, vasculitis, post-streptococcal
Post-renal is determined by renal ultrasound
234
How might a patient with CKD present?
May have hypervolemia, showing oedema, orthopnoea, crackles, high BP, cough, Raised JVP, dyspnoea and strong rapid pulse
Bloods show raised urea, creatinine and phosphate, as well as low albumin.
Often present with malnutrition, rash due to urea and phosphate, and pericardial rub due to extra serous fluid
Hb will be low due to RBC lifespan being exceeded
235
How do you confirm a diagnosis of CKD?
Look at kidney size
See if there is an obstruction
Decreased vitamin D
Hypoparathyroidism- decreased Ca2+ and increased P in the blood. Ca2+ is pulled out of bones
236
How do you treat CKD?
Most often focus on reducing GFP commonly using ace inhibitors. This treatment aims to stabilize the kidney function
237
What are the questions that should be addressed before giving IV fluids?
Is the patient euvolaemic, hypovolaemic or hypervolaemic?
Does my patient need IV fluid, and why?
How much?
What type (or type) of fluid is needed?
238
What are the types of IV fluid, and what do they do?
Hypotonic fluid pushes fluid into the cell and makes the cels fat
Hypertonic fluid pushes fluid out of cells and makes cells smaller
Isotonic fluids keep everything the same
239
How do we assess volume status?
Use JVP, oedema, weight gain and blood pressure
240
Why might a patient need or not need IV fluid?
Patients need an IV if they're not drinking, or have lost/losing fluid- to maintain, replace or recussitate. Fluid may be needed to replace that lost from blood or drains, diarrhoea, hyperemesis or third spaces (places where fluid shouldn't normally be)
They do NOT need an IV if they are drinking enough, on enteral feeding, or are already fluid overloaded
241
How much fluid do you prescribe per weight?
4ml/kg/hr for the first 10kg of weight
+2ml/kg/hr for the next 10kg of weight
+1ml/kg/hr for the remainder of body weight
242
When would you prescribe isotonic fluid?
Safest fluid- generally give this one unless it's maintenance for one that's already overloaded or with a high Na
243
Why would you prescribe hypotonic or hypertonic fluid?
For maintenance of high Na or fluid overloading patient
this pushes more water into the cells. Often 5% dextrose solution as dextrose is metabolised by cells and just becomes water
Hypertonic fluid is useful for severe hyponatremia
244
What causes hyponatraemia?
Mostly excess water
Sometimes sodium loss
Rarely pseudopyponatraemia (blood tests give false positives for hyponaturemia due to triglycerides or proteins being elevated)
245
What features can cause water excess and how?
Syndromes- ie cirrhosis, heart failure and nephrotic syndrome
SIADH as this causes water retention
Polydypsia (too much drinking)
246
How can you tell the difference between conditions causing water excess?
Use history- vomiting and diarrhoea, dehydration, medication
Examine fluid status
Check osmolarity
If osmolarity is normal then this is pseudohyponatremia
Fluid overloaded is a syndromal cause
Euvolemic is due to SIADH due to tumor, CNS, drugs and pneumonia, overhydration with hypotonic IV, diuretics due to drugs, Na+ loss and ADH activationor polydipsia (seen if urine osmolarity is low)
247
What is bad IV fluid selection and how can this cause harm?
If a hypotonic state occurs, the brain will likely swell, However, in a couple of days the body will adjust to fix this fluid imbalance by dragging solutes into the excess fluid - however, [Na+] is still low. If a hypertonic solution is given too quickly, osmolarity will increase hugely, causing brain shrinkage and herniation of the brainstem.
Generally, we treat sodium loss patients with saline, and water excess patients with fluid restriction
248
Where in the prostate do cancers occur? What types are able to form and why are they caused?
Occur in the transition zone around the urethra. This is the site of BPH and some cancers form here
Most occur in the peripheral zone of the prostate.
These cancers can be incidental and only found due to postmortem, or clinically important, with wide variation
Caused by genetics, or the environment
249
How do you diagnose a prostate cancer?
Digital rectal exam- feel a firm area or nodule
Trans-rectal ultrasound: can pick up new lumps. MRIs can pick up metastases
PSA is produced only in well differentiated tumors
A biopsy of the perineum or rectum can also show the cancer.
250
How do prostate cancers appear histologically? How are they classed?
They appear papillary
They can be graded from 1-5 based on their differentiation, and then the two most common histological pattern numbers are combined for a total score.
More recently, this has been changed to a combination of severity and score
251
How do prostate cancers progress?
Local spread, through extraprostatic fat, seminal vesicles and other pelvic structures- they spread via nerves
Lymph nodes can block of ureters etc.
Distant metastasis- esp. vertebral bodies
252
How are prostate cancers treated?
Low grade- no treatment
Significant- radical prostatectomy or radiotherapy
Advanced- palliative treatment like castration, anti-androgens, or local and metastatic radiotherapy
253
Describe bladder cancers
Mainly in males, smokers, industrial dye workers
Arises from transitional cell carcinoma in situ. Most present with haematuria, and are recurrent. They are followed up with urine cytology as well as cytoscopy
Macro cancers are mostly papillary and may invade
Microcancers are mainly urothelial, with some squamous
254
How do you treat bladder cancer?
Superficial cancers treated with local therapy and BCG
| Cancers into the detrusor muscle are treated with cystectomy
255
What are the main purposes of gynaecology?
To ease discomfort and disease, and to prevent disease, within the female genital tract
It also assists with reproduction and contraception
256
What are the important parts of patient interaction when seeing a gynaecology patient?
1. Take a proper history. As well as a general history, this includes menstrual history, contraceptives and side effects, and a sexual history.
2. Do a gynaecologic examination
3. Order tests
257
What should you focus on for heavy menstrual bleeding complaints, continence problems and lower abdominal pain in terms of history taking?
HMB: Talk about last menstrual period, regularity and flow of cycle, inter-menstrual bleednig, postcoital bleeding and medications
CP: Incontinence in terms of stress and urge, micturation problems, prolapse, previous UTIs etc.
Pain: SOCRATES, cyclicity, dyspareunia (pain with intercourse), as well as a menstrual history
258
Describe the typical gynaecologic examinations
First is a general and abdominal exam. See if the patient is uncomfortable/distressed. Follow with abdominal exam, to see if there are masses or tender areas. Sometimes do a breast exam on older patients
Pelvic examination and speculum- start with vulva, then vagina, then speculum. Use the handle facing downwards if the patient i in the lithotomy position, or up if the patient is simply on a bed.
Then a digital examination- two fingers into the vagina to feel the uterus size, masses and tenderness. If the uterus is fixed, there could be scarring or fibroids involved.
259
What are some common gynaecologic investigations?
Urine tests, cervical smears (check cell type in cervix), vaginal swabs (suggest infection and tenderness), biopsy of endometrium, ultrasound to check endometrial thickness, and bloods to check for anaemia
260
What are the possible causes of heavy menstrual bleeding?
Structural causes = PALM (papilloma, adenomyosis, leioma or Malignancy)
Non-structural causes = COIENT: Coagulopathy, ovulatory dysfunction, endometrial, iatrogenic, not classified, thyroid disease
261
Describe leiomas (fibroids)
They are common and estrogen dependent
They are benign leiomyomata arising from the uterine myometrium
They present with abnormal uterine bleeding, pelvic discomfort but no pain
Can be treated conservatively, with NSAIDS, mirena IUDs and GnRH analogues, or invasively with a myomectomy, hysterectomy or uterine artery embolism.
262
Describe how acute heavy menstrual bleeding is treated
Normally use high dose progestogens or tranexamic acid to stop the bleeding
Oral contraceptives control it, although should consider DVT risk
If there's no pathology, and 3mos of treatment has failed, then endometrial ablation may be necessary, or even a hysterectomy
263
How do you treat incontinence in women?
Determine type of incontinence- may be overflow due to urethral blockage, stress due to a relaxed pelvic floor and increased abdominal pressure, or urge, where the bladder is oversensitive
Stress needs weight loss, smoking cessation, decreased caffeine or pelvic floor therapy. Urge tends to be more bladder training
264
What is endometriosis and how is it treated?
It's the presence of endometrial tissue where it shouldn't be. This means when the lining is sloughed off women end up bleeding into their pelvic cavities as well, causing pain due to inflammation
Treated with pain management, hormonal suppression, potential laparoscopic excision of endometrial deposits and potentially a historectomy
However, it often recurs, although it regresses in pregnancy and postmenopause
265
How do you use your hands when dealing with labour?
Find the fetal lie (long axis of fetus in relation to uterus
Find the baby's size and gestational age by measuring from pubic symphysis to the fundus
Find presentation by palpating. Can be cephalic, breech or shoulder
Find fetal engagement- how deeply the presenting part is engaged in the bony pelvis
266
How do you use your ears when dealing with labour?
Take a fetal heartbeat
| Ask about the baby's movements
267
How can you tell whether true labor has started?
The mother experiences painful uterine contractions, accompanied by effacement (thinning) and dilation of the cervix
268
What are the different stages of labour?
First stage is the opening of the cervix to full dilation
Second stage is full dilation to delivery
Third stage is delivery of baby to delivery of placenta
269
What are the mechanical determinants of a successful labor?
Passenger
Passage
Power
270
Describe how 'passenger' affects birth
Diameter of the baby's head. The bones are not yet fused, and have sutures and fontanelles. The occiput should be the lead point of the head. Through the pelvis, the head is first transverse as it moves through the upper pelvis, and rotates around to anteroposterior as it moves through the thinner lower pelvis.
For the most part, the head should be flexed, as extension widens the head's diameter
271
Describe how 'passage' affects birth
The inlet of the pelvis is wider in the transverse plane, mid-cavity is round, and the outlet is wider in the AP plane.
The ischial spines can also be used as a comparative tool to determine how far the baby's head is from them
272
Describe how 'power' affects birth
Contractions push the baby down and pull the cervix open
| They should last for 45-60 seconds, and come every 2-3 minutes
273
Describe normal labour
Contractions can be braxton hicks- normal in late gestation
Prostaglandins and oxytocin are released, softening the cervix and initiating contraction
First stage involves regular contraction, effacement and dilation (first 3 cm is latent phase, 3-10 cm is active phase). This should occur at a rate of about 1cm/h for a first time mother
Fetal descent, flexion and rotation as well as rupture of the membranes should also occur
Second stage involves completed descent, flexion and rotation. Active stage starts when mother has irrepressible desire to push
Delivery occurs wth extension of the baby's head around the symphysis, and then rotating back to the transverse position
Third stage involves placental delivery
274
Describe active and passive methods of delivering the placenta
Active- give acbolic injection, clamp and ligate cord, give traction
Passive (more risky)- don't clamp and traction cord, maternal effort expels the placenta
275
Describe abnormal labour and what can cause it
Slow progress or prolonged labour
Due to insufficient uterine action (can be augmented with oxytocin), fetal size, disorder of rotation (baby's occiput is transverse or posterior), or cephalo-pelvic disproportion
276
What are the different types of instrumental delivery?
Can use forceps- quicker, but more maternal injury and neonatal facial nerve palsy
Can use ventouse- possible to rotate, though more cephalhaematomas
Note that the baby has to be past the narrowest point for instrumental delivery
277
Why would you perform a caesarian?
Due to obstructed labor, or to because of maternal or fetal concerns
278
Define metaplasia
Change of cells to a form that does not normally occur in the tissue they are found in
279
Define dysplasia
Abnormal development of cells, typically indicative of an early neoplastic process. Normally restricted to the originating tissue (in situ if full thickness of tissue)
280
What are the different categories of change that can occur in a pathological ovary?
Non-neoplastic pathologies can be polycystic ovarian syndrome, or functional ovarian cysts
Benign tumours can be epithelial (mucous or serous cystadenomas), germ cell (teratoma) or stromal (fibroma) in nature
Malignant tumours can be primary (ovarian carcinoma) or secondary (metastatic carcinoma)
281
Describe the features of serous carcinoma
Shows large, malignant cells and restructuring of ovarian tissue
282
Describe the function of the fallopian tubes
The fimbrae align over the released follicle, which enters the lumen and is fertilized. Ciliated cells push the ovum towards the uterus
283
Describe the types of pathology of the fallopian tubes
Non-neoplastic can be salpingitis or ectopic pregnancy
Pre-malignant can be tubal intraepithelial carcinoma
Benign can be an adenomatoid tumour
Malignant can be primary carcinoma, or a secondary metastatic carcinoma
Most arise from the distal end of the tube in the epithelial lining
284
Describe the function of progesterone and estrogen in the uterus
Estrogen causes the proliferative stage of endometrial development
Progesterone causes secretory endometrial development
285
Describe the types of pathology that can develop in the uterus
Endometrial: Non neoplastic can be endometritis and edometriosis, pre-malignant is hyperplasia, benign is endometrial polyms or malignant is endometrial adenocarcinoma or stromal sarcoma
Myometrial: Non-neoplastic is adenomyocis (endometriosis), benign is leiomyoma (fibroid) and malignant is leiomyosarcoma
286
Describe the types of pathology found in the cervix
Non-neoplastic is cervicitis or candida
Pre-malignant is squamous intraepithelial lesions or adenocarcinoma in situ
Benign is endocervical polyp
Malignant is squamous cell carcinoma or adenocarcinoma
287
Describe how CINs are graded
CINs are cervical intraepithelial neoplasia (squamous intraepithelial lesions)
Low grade are only 1/3 through the epithelium (CNI), CNII is through 2/3, and CNIII is through the whole layer. This type of cancer can't metastasize as it hasn't yet broken through the basement membrane to the blood.
They eventually go on to have further mutations allowing for invasion.
288
What are some congenital abnormalities of the female reproductive tract?
Intersex
Malformed uterus
Abnormalities in ovarian development
289
Describe the HPV virus and its risks
It's an often transient, self limited virus that can be associated with CIN
Viral factors, as well as lifestyle factors, account for its risk
290
What are the two main categories of sexual problems?
One is impairments to physiology
| The other is impairments in the human relations part of sex
291
Describe non-physiological sexual dysfunction and the model that assists it
It can be interpsychic (issues with relationships) or intrapsychic (issues with self view)
Can also be social, in terms of situational (ie there's a window)
It's able to be treated in accordance with the plissit model, which involves 4 levels of complexity
Permission to discuss/explore sexuality
Limited information
Specific suggestions
Intensive therapy
292
Describe female sexual dysfunction
Low desire, orgasmic disorder or pain/penetration disorder. Must be experienced most of the time for at least 6mos, and causing significant distress
It can be treated with counselling, and managing any medical problems
293
Describe male sexual dysfunction
Hypoactive sexual desire, erectile disorder or premature ejactulation Must be experienced most of the time for at least 6mos, and causing significant distress
Can be caused by psychological, physical or other causes
294
What can be associated with male and female sexual dysfunction?
Partner issues, relationship issues, individual vulnerability, cultural, religious or medical factors
295
How does erection normally occur and resolve?
Normally, the brain sends signals to release NO, which increases cGMP. This causes smooth muscle relaxation in associated arteries, allowing them to swell and compress the veins, preventing flaccidity
Eventually, PDE5 destroys cGMP and limits the erection
296
What is erectile dysfunction and how is it managed?
It's a persistent inability for at least 6mos to obtain and maintain an erection sufficient for satisfactory sexual performance.
Can be organic or psychogenic, due to age, illness, surgery or trauma
Managed by managing co morbidities, adjusting medication and lifestyle, educating and sometimes treating
297
What are some examples of PDE5 inhibitors and what do they do?
Sildenafil is viagara, tadalafil has a longer low dose duration
These inhibit PDE5, allowing a longer erection
298
What is premature ejaculation and what can help resolve it?
Ejaculation before the individual desires
| Can be treated with SSRIs
299
What is delayed ejactulation, what causes it and how can it be treated?
No actual definition- is situational
Mostly attributed to fear, anxiety etc. Now recognized as due to hypofunction of some serotonin receptors, so decreased serotonins are needed to counteract this. It involves taking SSRI patients onto a lower or different medication
300
What are the different kinds of scrotal masses?
Can be testicular (neoplastic or non-neoplastic)
Can also be non-testicular, eg. hernia, hydrocoele, haematocoele or edpididymis issues
They can present with enlarged or irregular testes, metastases or hormonal issues
301
What are the different types of testicular germ cell tumour and where do they come from/grow?
They can be malignant germ cell tumours or testicular tumours- most are crossed over between both, creating testicular germ cell tumours
However, there are exception: Malignant ovarian GCTs and midline GCTs are only malignant, whereas lymphomas and sertoli/leydig cell tumours are only testicular
They come from totipodent cells, and may grow in the testis, or midline sites such as the mediastinum, pineal gland, sacrococcyx
302
How are testicular GCTs classified?
Can be seminoma (poor differentiation), non-seminomatous GCTs (later in life) or combined
May be embryonal carcinoma, teratoma, choriosarcinoma or yolk sac tumour
A seminoma is formed from gonadal germ cell differentiation
Embryonic differentiation causes teratoma (from ecto, meso and endoderm), choriosarcinoma (from trophoblast) and yolk sac tumour (from extra-embryonic mesoderm
303
What can cause germ cell tumours?
Genetic factors, like ethnicity or cryptorchidism
Gonadal dysgenesis (female but testes instead of ovaries
Intratubular germ cell neoplasia: causes increased copies of 12p- when other chromosonal issues happen, we see seminoma and NSGCTs (not pediatric or spermatocytic seminoma)
304
How do GCTs appear on a macroscopic level?
They expand and replace normal testicular tissue
They remain confined within the tunica albuginea
Seminomas appear a homogeneous, granular cream
Teratomas have cartilage, cysts, creat/grey necrosis
Choriocarcinomas have haemorrhage
Yolk sac tumours are grey and gelatinous
305
How do you diagnose and stage testicular tumours
Diagnose with clinical examination, ultrasound to confirm, inguinal orchidectomy and pathological examination
Staged using chest Xray, CT and serum tumour markers
306
How do GCTs spread?
Local invasion to rete testis and epididymis is uncommon
| Mostly lymphatic invasion and haematogenous (to lung, liver and others)
307
What are tumour markers and how do they indicate the tumour type?
Can have HCG- produced by trophoblast and -derm cells, so can indicate choriocarcinoma, malignant teratomas and some seminomas
AFP is produced by -derm and extra-embryonic endoderm so can indicate malignant teratoma or yolk sac tumours
308
How do you manage testicular tumours after orchidectomy?
Seminoma with minimal node involvement- light radiotherapy
Seminoma with lots of nodal involvement- platinum based chemo
NSGCT: intensive surveillance. Exams using Xray, CT, markers/ Treat recurrences with platinum chemo
309
What are some diseases of the penis? When might carcinomas occur?
Skin diseases
Venereal diseases
Squamous cell carcinoma: occurs in the elderly, HPV. Protected by circumcision
Can target glans and coronal sulcus, may spread to inguinal nodes and once they invade the spongy tissue, metastasis is more likely
310
What is a dermoid cyst (teratoma) and how does it present in the ovary?
It is a tumor derived from germ cells which comprises a variety of mature tissues from ectoderm, mesoderm and endoderm, such as skin, brain, muscle, hair tissue. They are only occasionally malignant.
They present with pain and large cystic mass on ultrasound. Can be stained with haematoxylin and eosin
311
What is a cystadenoma and how does it present in the ovary?
It can be mucinous or serious (mucinous or tubal epithelium), and can appear at multiple age ranges unilaterally, and a variety of sizes. It can be benign (simple structure) borderline (CIS with displasia) or malignant
Presents with pain, gradual swelling and large adnexal mass
312
Describe infection of the fallopian tubes and how it presents
It is usually a bacterial infection, but can also be parasitic or TB infection of the fallopian tubes.
Can be due to endometritis, salpingitis, oophoritis and peritonitis, as well as abcesses and cysts
It results in abnormal bleeding, vaginal discharge, fever pain, infertility and cysts
313
Describe ectopic pregnancy and how it presents
Fetus fomation in the cervix/fallopian tubes/peritoneal cavity
Presents with severe pain, bleeding and amenorrhea, as well as adnexal mass, elevated hCG, and empty uterus
Can show dilated fallopian tube/rupture
314
How do leiomyomas and leiomyosarcomas present? What are they?
Leiomyomas are benign smooth muscle tumours. They are common and receptive to hormones, so often regress after menopause
Leiomyosarcomas are the malignant equivalent
Present with enlarged (benign) or pleiomorphic (malignant) nuclei, urinary frequency, menorrhagia and dysmenorrhoea
315
Describe how endometriosis presents in the ovary
Presents with infertility, cyclical abdominal pain, haematuria.
On laparoscopy, can see 'chocolate cysts' in the ovary, and cysts on the uterus.
This is a problem as it bleeds into the adjacent tissue, causing pain, cysts, inflammation, infertility and ectopic pregnancy
It also gives rise to malignancy
316
Describe endometrial carcinoma and how it presents
Glands proliferate and merge due to increased estrogen exposure. This causes dysplasia
Treated with total hysterectomy, bilateral salpino-oophorectomy
Presents with heavy, irregular periods and thickened endometrium
317
What factors predispose to endometrial carcinoma
Obesity, hormone replacement therapy, polycystic ovarian syndrome, hormone secreting tumours, early menarche or late menopause, nulliparity
318
Describe the different types of cervical smear and how each should be managed?
Can show cells with normal nuclei- normal smear just needs regular 3 yearly smears
Can show low grade dysplasia with slightly enlarged nuclei (takes up 1/2 cell)- next smear in 1 year to see if infection has cleared spontaneously etc
Can show high grade dysplasia, where nucleus takes up most of cytoplasm. Send to specialist for biopsy, surgery, other treatment. Follow up with annual smears
319
How do you do a cervical smear?
cytobrush takes cells from endo, ecto and transitional cervix
