Deck 2 - GU Flashcards
Q. Describe the histological epithelium change in bladder cancer
A. Transitional epithelium to squamous bladder cancer
Q. Name three risk factors associated with bladder cancer
A. Smoking (50%), occupational exposure to carcinogens (rubber, leather, metal, worker, plastics, azo dyes), age, gender, family Hx, HNPCC for upper tract urothelial cancers
Q. Name two symptoms associated with bladder cancer and two investigations
A. LUTS: painless haematuria, dysuria, abdo pain, weight loss/bony pain,
B. Urine dipstick, FBC, flexible cystoscopy, upper tract imaging (CT, USS, XR)
C. Imaging: USS renal tract or CT IVU
Q. How is bladder cancer graded? (which investigation)
A. TURBT: trans-urethral resection of bladder tumour
B. For histological grade and stage
C. Tis: carcinoma in situ
D. Ta: non-invasive papillary carcinoma
E. T1: tumour invades in subepithelial connective tissue
F. T2a: invades superficial muscle
G. T2b: tumour invades deep muscle
H. T3: tumour invades perivesical tissue
I. T4: tumour invades adjacent tissue and organs
Q. Name some treatments of bladder cancer
A. Muscle invasive: surgery, metastatic work up, oncology consult for neoadjuvant chemotherapy, radiotherapy
B. Carcinoma in situ: intravesical Bacilli Calmette-Guerin (BCG), follow up cytology
C. Other non-muscle-invasive lesion: TURBT if not completely excised, follow-up
Q. What is the main site of renal reabsorption? Which condition is associated with pathology in this location?
A Proximal convoluted tubule
B Fanconi syndrome
Q. Which renal site do loop diuretics target?
A. The loop of Henle (Normally Na is reabsorbed in the ascending limb and water is reabsorbed in the descending limb). Loop diuretics block the movement of sodium, and therefore, water.
Q. Name two physiological factors that can affect potassium filtration and absorption
A. Distal delivery of sodium
B. Aldosterone
C. (Insulin and catecholamine’s drive cellular K+ uptake)
Q. Describe the mechanisms of ACE-inhibitors and angiotensin II receptor blockers in CKD
A. ACE-I: affects RAAS, preventing the formation of aldosterone – (therefore preventing increases in BP)
B. ARB: blocks angiotensin receptors (preventing increases in BP)
Q. How does aldosterone regulate salt levels?
A. Aldosterone increases sodium reabsorption by increasing the production of ENaC channels in the collecting duct
Q. What hormone controls the permeability of the collecting duct to water? What mechanism is this associated with?
A. ADH (or argininevasopression) controls permeability of collecting duct to water:
B. Vasopressin: increases Aquaporin 2 molecules (AQP2) in apical membrane via G-protein coupled cAMP-mediated process: increasing H20 transport
Q. Which hormones increase excretion of sodium and water and which decrease it?
A. Aldosterone decreases excretion (favours water reabsorption by production of ENaC channels in the collecting duct)
B. Angiotensin II decreases excretion
C. ANP - atrial natriuretic hormone - increases excretion by increasing GFR and decreasing na reabsorption in the DCT and collecting duct
Q. What occurs in nephrogenic diabetes insipidus? Name 3 symptoms/clinical features
A. Renal damage results in insufficient levels of ADH/vasopressin, this decreases the kidney’s ability to concentrate urine by reabsorbing water
B. Symptoms: excessive thirst, dehydration, incontinence secondary to chronic bladder distension, polyuria (excretion of over 2.5L urine per day), neuro symptoms may occur if patient is unable to drink (hypernatremia)
Q. Name two causes of nephrogenic diabetes insipidus
- Q. Name two causes of nephrogenic diabetes insipidus
A. Hypercalcaemia (most common cause – causes natiuresis – increased sodium loss in the urine and water diuresis)
B. Hypokalaemia, lithium, genetic (rare)
Q. What is the exocrine function of the kidney in response to hypoxia?
A. Release of erythropoietin – increase Hb production
