Phase II - GU Flashcards
What might dysuria suggest?
Inflammation.
Give 3 causes of nocturnal polyuria.
- Habitual.
- Congestive cardiac failure.
- Sleep apnea.
Give a surgical treatment for BPE.
TURP.
What nerve fibres do cavernous nerves carry?
Parasympathetic: S2-4.
Sympathetic: T11-L2.
Describe the physiology of an erection.
- Parasympathetic stimulation.
- Arteriolar dilation.
- Smooth muscle relaxation.
- Testosterone.
What chemical compound is responsible for the smooth muscle relaxation that is required for an erection?
Nitric oxide (NO). It causes a fall in cytoplasmic calcium -> smooth muscle relaxation.
What are the 2 main causes of erectile dysfunction?
- Organic e.g. vasculogenic, neurogenic, hormonal, anatomical.
- Psychogenic.
Give 3 characteristics of psychogenic erectile dysfunction.
- Sudden.
- Situational.
- Younger males affected.
Give 4 risk factors for erectile dysfunction.
- Obesity.
- Lack of exercise.
- Smoking.
- Diabetes mellitus.
What is the non-pharmacological management of erectile dysfunction?
- Lose weight, stop smoking.
2. Education and counselling of patient and partner.
What is the first line pharmacological management of erectile dysfunction?
Phosphodiesterase inhibitors e.g. viagra, cialis. They cause vasodilation and so increase arterial blood flow to the penis.
What is the second line pharmacological management of erectile dysfunction?
- Intracavernous injections.
2. Vacuum devices.
What is the third line pharmacological management of erectile dysfunction?
Penile prosthesis implantation.
What is priapism?
Prolonged erection, lasting for >4 hours.
What is a potential consequence of priapism?
Permanent ischaemic damage.
Give 5 functions of the kidney.
- Filters and excretes waste products from the blood.
- Regulates BP.
- Retains albumin.
- Reabsorption of Na, Cl, K, glucose, H2O, amino acids.
- Synthesises EPO.
- Converts 1-hydroxyvitaminD to 1,25-dihydroxyvitaminD.
Write an equation for GFR.
(Um X urine flow rate) / Pm.
- Um = concentration of marker substance in urine.
- Pm = concentration of marker substance in plasma.
What would you expect a typical GFR to be?
120ml/min.
Give an example of a marker substance used for estimating GFR.
Creatinine.
Estimating GFR: Give 3 essential features of a marker substance.
- Not metabolised.
- Freely filtered.
- Not reabsorbed/secreted.
Name a drug that can inhibit creatinine secretion. What is the affect of this on GFR?
Trimethoprim.
Serum creatinine rises and so kidney function (GFR) appears worse.
What is the affect on GFR of afferent arteriole vasoconstriction?
Decreased GFR.
What is the affect on GFR of efferent arteriole vasoconstriction?
Increased GFR.
Where in the nephron does the bulk of reabsorption occur?
At the proximal convoluted tubule.
What 7 things are reabsorbed at the PCT?
- Sodium.
- Chlorine.
- Potassium.
- Glucose.
- Water.
- Amino acids.
- Bicarbonate.
What is Fanconi syndrome?
Failure of the nephron to reabsorb essential ions. Sugar, amino acids and bicarbonate are therefore present in the urine.
Give 2 signs of Fanconi syndrome.
- Sugar in the urine.
- Acidotic due to bicarbonate in the urine.
- Rickets/osteomalacia.
Give 2 causes of Fanconi syndrome.
- Myeloma.
2. Cystinosis.
What is the function of the counter current multiplication system?
It generates a hypertonic medullary interstitium for H2O reabsorption. Na+ moves out of the ascending limb which increases the medullary osmolality, H2O follows.
Which part of the loop of henle is permeable to H2O?
The descending limb is permeable to H2O.
Describe tubuloglomerular feedback.
Macula densa cells of the DCT lie between the AA and EA. They detect NaCl and use this as an indicator of GFR.
Macula densa cells detect a raised NaCl. What is the response?
AA constriction.
Macula densa cells detect a reduced NaCl. What is the response?
Renin secretion.
What 2 cell types are found in the nephron collecting duct?
Principal and intercalated cells.
What hormone is responsible for regulating sodium reabsorption?
Aldosterone.
Why might aldosterone secretion lead to hypokalaemia?
Aldosterone secretion leads to increased sodium reabsorption. Sodium reabsorption leads to increased potassium secretion and therefore hypokalaemia.
What is the affect of NSAIDs on the afferent arteriole of glomeruli?
NSAIDs inhibit prostaglandins and so lead to AA vasoconstriction = reduced GFR.
NSAIDs lead to a reduced GFR. Why?
NSAIDs inhibit prostaglandins and so lead to afferent arteriole vasoconstriction -> reduced GFR.
What is the affect of ACEi on the efferent arteriole of glomeruli?
ACEi cause EA vasodilation = reduced GFR.
Name 2 factors that govern renal potassium.
- Na+.
2. Aldosterone.
What ion is responsible for volume control?
Sodium!
Name 2 hormones that increase sodium reabsorption.
- Aldosterone.
2. Angiotensin 2.
Name a hormone that decreases sodium reabsorption.
ANP.
What is the function of EPO?
It stimulates the bone marrow -> RBC maturation.
Give 2 functions of calcitriol.
- Increased calcium and phosphate absorption from the gut.
2. Suppression of PTH.
What triggers PTH secretion?
Low serum calcium.
Give 3 ways in which PTH increases serum calcium.
- Increased bone resorption.
- Increased reabsorption of calcium at the kidneys.
- Stimulates 1-hydroxylase -> 1,25-dihydroxyvitaminD -> increased calcium absorption from the intestine.
Name 2 hormones secreted from the posterior pituitary gland.
- ADH.
2. Oxytocin.
Describe the function of ADH.
ADH acts on the collecting ducts. It increases insertion of aquaporin 2 channels leading to H2O retention.
Give 3 factors that stimulate renin release.
- Sympathetic stimulation.
- Decreased BP.
- Decreased Na detected by macula densa.
Give 3 functions of ANP.
- Renal vasodilator.
- Inhibits aldosterone.
- Closes ENaC (decreased reabsorption of Na+).
Where on the nephron does aldosterone act?
On the collecting ducts.
Describe aldosterone action.
Aldosterone acts on the collecting ducts. It increases ENaC and H+/K+ pumps. There is increased Na+ absorption and K+ secretion -> H20 retention -> increased BP.
Define urinary tract infection.
Inflammatory response of the urothelium to bacterial invasion, usually associated with bacteriruria and pyuria.
Name 2 groups of people that you would treat for bacteriuria?
- Pregnant ladies.
- Children.
What is septic shock?
Severe sepsis with persistent hypotension.
Describe the pathophysiology of urosepsis.
A symptomatic UTI combined with >1 of: 1. Microbial resistance. 2. Immunosuppression. 3. Pressure. = UROSEPSIS!
What can cause raised urinary tract pressure?
- Stone in lumen of UUT.
- Tumour in the wall.
- LUT outflow obstruction: BPH, tumour, stone.
- Bladder dysfunction.
Give 4 causes of urinary tract colonisation.
- Diseases that require steroids or chemo e.g. diabetes, immunodeficiency.
- Stones or tumour in the lumen of the urinary tract.
- Poor bladder emptying.
- Catheterisation.
Describe the treatment for sepsis.
The sepsis 6:
- Give high flow oxygen.
- Take blood cultures.
- Give IV abx.
- Give IV fluids.
- Check lactate.
- Monitor hourly urine output.
Also drainage to relieve pressure!
Name the classification that helps differentiate between benign cystic lesions and cancerous cystic lesions.
The Bozniak classification.
A patient presents with haematuria. A MSU sample is taken and a blood film is done. The RBC’s look dysmorphic. Where in the urinary tract is the problem likely to be?
Dysmoprhic RBC’s signify a glomerular origin.
If the RBC’s looked normal the problem is likely to be with the LUT.
Give 5 causes of haematuria.
- Kidney tumour, trauma, stones, cysts.
- Ureteric stones or tumour.
- Bladder infection, stones or tumour.
- BPH or prostate cancer.
What further investigations might you do in someone who presents with haematuria?
- Urinalysis.
- Urine cytology.
- Abdomen US.
- Abdomen CT.
- Cystoscopy.
Describe the fluid distribution in the body.
ICF: 28L.
ECF: 14L
- Interstitial: 11L.
- Plasma: 3L.
Total body water: 42L.
How much extra-vascular fluid is there in the body?
ICF + interstitial = 39L.
How much intra-vascular fluid is there in the body?
Plasma: 3L.
What happens to the heart rate in hypovolaemia?
Increases - tachycardia.
What happens to the blood pressure in hypovolaemia?
Decreases - hypotension.
What happens to the JVP in hypovolaemia?
JVP is low.
What happens to tissue turgor in hypovolaemia?
Tissue turgor is reduced.
What happens to urine output in hypovolaemia?
Urine output is reduced.
What happens to weight in hypovolaemia?
Weight is reduced.
Give 2 symptoms of hypovolaemia.
Thirst and dizziness.
What happens to creatinine, haemoglobin and haematocrit levels in hypovolaemia?
They are raised.
Name 5 groups of people who are at risk of hypovolaemia.
- Elderly.
- Those who have had an ileostomy.
- People with short bowel syndrome.
- Bowel obstruction.
- People taking diuretics.
Name 5 groups of people who are at risk of hypervolaemia.
- Acute kidney injury patients.
- CKD patients.
- Heart failure patients.
- Liver failure patients.
What happens to the heart rate in hypervolaemia?
HR is normal.
What happens to blood pressure in hypervolaemia?
Blood pressure is high or normal.
What happens to JVP in hypervolaemia?
JVP is high.
What happens to tissue turgor in hypervolaemia?
Tissue turgor is normal.
What happens to urine output in hypervolaemia?
Urine output is normal.
What happens to weight in hypervolaemia?
Weight is increased.
Give 2 symptoms of hypervolaemia.
- Shortness of breath.
2. Peripheral oedema.
What happens to creatinine, haemoglobin and haematocrit levels in hypervolaemia?
They are reduced.
Where might fluid accumulate in someone with hypervolaemia?
- Pulmonary oedema.
- Pleural effusion.
- Ascites.
- Bowel obstruction.
- Intra-abdominal collection.
Describe the management for hypovolaemia.
- Oral fluid.
- IV fluid if very ill.
- Treat reversible causes.
Describe the management for hypervolaemia.
- Diuretics e.g. furosemide.
- Fluid restriction.
- Treat reversible causes.
Name 3 isotonic solutions.
- 5% dextrose.
- 0.9% NaCl.
- Hartmann’s solution.
What type of IV fluid moves from the intra-vascular to the extra-vascular space?
Crystalloid.
Small molecules pass through cell membranes and so move from the intra-vascular to extra-vascular space.
Give an example of a colloid IV fluid.
Gelofusine.
Give 3 potential causes of rising creatinine.
- Too aggressive with diuretics.
- Extravascular hypervolaemia but intravascular hypovolaemia.
- Progression of CKD.
Describe the pathophysiology of congenital polycystic kidney disease.
Genetic mutation -> predisposition to cyst development -> cell proliferation and loss of planar polarity -> fluid secretion and cyst expansion.
Describe the pathophysiology of acquired polycystic kidney disease.
Cysts develop over time.
Renal injury/ischaemia -> abnormal cell proliferation.
What classification can be used to help differentiate between benign cystic lesions and cancerous lesions?
Bozniak classification.
Give 4 congenital causes of renal cysts.
- ADPKD.
- ARPKD.
- VHL.
- OFD1 (oral-facial-digital syndrome 1).
A mutation in what gene can cause ARPKD?
PKHD1.
Give 4 features of acquired renal cystic disease.
- No genetic mutation.
- No family history.
- Normal kidney size.
- Risk factor for renal cell carcinoma.
What is the access point in haemodialysis?
AV fistula.
Why might someone having haemodialysis have a PFTE graft as opposed to an AV fistula?
If the patient has atherosclerotic veins or has had previous fistulas they may have a PFTE graft or a catheter tunnelled into the RA.
Give examples of waste products that are removed from the blood in dialysis.
- Urea.
- Creatinine.
- Potassium.
- Phosphate.
How many times a week and for how long does someone have hospital haemodialysis for?
3-5 hours, 3 times a week.
How many times a week and for how long does someone have home haemodialysis for?
2-3 hours, 4-5 times a week.
Why can someone on home haemodialysis take fewer tablets and have less dietary restrictions compared to someone on hospital haemodialysis?
Patients doing home haemodialysis dialyse more frequently and so can have less restriction on their diet.
Give 5 potential complications of haemodialysis.
- Hypotension.
- Cramps.
- Nausea.
- Chest pain.
- Fever.
- Blocked or infected dialysis catheter.
Give 3 groups of people who haemodialysis is good for.
- People who live alone/frail/elderly.
- People who fear operating machines.
- People who are unsuitable for PD e.g. previous abdominal surgery, abdominal hernia etc.
What is the access point in peritoneal dialysis?
A peritoneal catheter is placed into the peritoneal cavity through a SC tunnel.
How often does someone have to do CAPD?
30-40 minute exchanges, 3-5 times a day.
How often does someone have to do APD?
One exchange overnight (8 hours).
Give 4 potential complications of peritoneal dialysis.
- Infection e.g. peritonitis/catheter exit site infection.
- Peri-catheter leak.
- Abdominal wall herniation.
- Intestinal perforation.
Give 3 groups of people who peritoneal dialysis is good for.
- Young people/those in full time work.
- People who want control/responsibility of their care.
- People with severe HF.
Where in the abdomen does a transplanted kidney lie?
In the iliac fossa.
Describe the criteria for selection of a living donor for kidney transplant.
- Blood relative.
- ABO blood group compatible.
- HLA identical.
- Excellent medical condition and normal renal function.
Name 3 medical conditions that can exclude living kidney donation.
- Renal parenchymal disease.
- History of stones/frequent UTI/hypertension/DM.
- Recent malignancy.
Describe the criteria for selection of a cadaver donor for kidney transplant.
- Irreversible brain damage.
- Normal renal function.
- No evidence of pre-existing renal disease or transmissible disease.
- ABO compatible and best HLA possible.
What tests can be done to evaluate kidney function in a potential kidney donor?
- Serum creatinine.
- Creatinine clearance.
- Urinalysis.
- Urine culture.
- GFR.
Give 5 contraindications for renal transplant.
- ABO incompatibility.
- Cytotoxic Ab’s against HLA antigens.
- Recent malignancy.
- Active infection.
- AIDS.
- Morbid obesity.
- Age > 70 y/o.
Give 3 ways in which recipient and donor matching is assessed.
- HLA tissue typing (important to match DR antigens).
- Lymphocytotoxic cross matching; checks there are no preformed antibodies against HLA antigens.
- ABO blood group compatibility.
Give 4 factors that can influence the longevity of renal allograft.
- Age.
- HLA matching.
- Ischaemia time.
- Number of acute rejection episodes.
- Ethnicity.
What are the 2 major causes of allograft failure?
- Chronic rejection.
2. Death with functioning graft.
What are the 2 major causes of death after kidney transplant?
- CV disease.
2. Infection.
Name the 3 types of renal allograft rejection.
- Hyper-acute.
- Acute.
- Chronic.
Describe hyper-acute renal allograft rejection.
Preformed antibodies against HLA antigens of donor organ.
Why might someone have pre-formed antibodies against HLA antigens?
Can be a consequence of blood transfusion, pregnancy, prior transplant, auto-immune disease.
What can cause immediate graft loss?
Fibrinoid necrosis.
Describe acute renal allograft rejection.
Activated T lymphocytes. Occurs within the first 6 months but is often reversible e.g. with steroids.
Describe chronic renal allograft rejection.
Slow and gradual decline in renal function, accompanied by proteinuria.
What criteria can be used to diagnose allograft rejection?
Banff criteria.
Give 3 consequences of chronic immunosuppression.
- Malignancy.
- Infection.
- SE’s of other drugs.
Give 3 consequences of glomerulonephritis (glomerular disease).
- Leaky glomeruli -> haematuria and proteinuria.
- High BP.
- Deteriorating kidney function.
Briefly describe the pathophysiology of glomerulonephritis (glomerular disease).
Immunologically mediated: immunoglobulin deposits and inflammatory cells.
Name a loop diuretic.
Furosemide - acts on Na+/K+/2Cl- transporter (NKCC2).
Give 3 potential side effects of furosemide.
- Hypokalaemia.
- Hypotension.
- Dehydration.
What other drug might you prescribe with furosemide in someone with poorly controlled potassium?
A potassium sparing diuretic e.g. spironolactone. These work on RAAS (hormonal systems) as opposed to ion channels and should help control potassium levels in the blood.
Name a potassium sparing diuretic.
Spironolactone.
On which part of the nephron do thiazides act?
The distal tubule.
Act on NCC channels.
A 50 y/o M presents with haematuria. On examination he has HTN, increased serum Cr and urea, proteinuria and bilateral palpable costo-vertebral angle masses. You take a family history and find out that his dad died of a sub-arachnoid haemorrhage. What is the most likely diagnosis?
ADPKD.
- Normally people present around 50 y/o.
- Raised creatinine and urea indicate a kidney problem.
- The kidneys can be HUGE in ADPKD hence the palpable masses.
- Intracranial haemorrhages are an extra-renal manifestation of ADPKD.
What is the most common renal cancer in children?
Wilms tumour.
What drug must you not give to someone with renal artery stenosis?
ACE inhibitors e.g. ramipril.
