Urogenital Flashcards

1
Q

what are the antidotes to teh following drug overdoses - Anti-freeze (ethylene glycol) poisoning –
Cyanide poisoning –
Lead poisoning –
Organophosphate poisoning – A
Heparin overdose –

A

Anti-freeze (ethylene glycol) poisoning – Ethanol
Cyanide poisoning – Dicobalt edetate
Lead poisoning – Sodium calcium edetate
Organophosphate poisoning – Atropine
Heparin overdose – Protamine sulphate

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2
Q

Nephrolithiasis definition

A

the prescence of stones in teh renal system

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3
Q

Nephrolithiasis epidemiology

A
  • Typically 30-60 years old
  • M>F
    50% lifetime risk of reoccurrence
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4
Q

Nephrolithiasis risk factors

A
  • Dehydration
  • Previous stones
  • stone forming foods
  • Genetic - renal tubular acidosis
  • Metabolic - hypercalcaemia, hyper parathyroidism, hypercalciuria
    Family history
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5
Q

Nephrolithiasis pathophysiology

A
  • Solutes in the urine precipitate and crystalise and form a stone. Substances like magnesium and citrate inhibit the crystal growth
  • Calcium oxalate is the most common renal stone formation - acidic urine
  • Calcium phosphate - more liley to form in alkalaine urein
  • Uric acid - this doesn’t show up on x ryas
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6
Q

Nephrolithiasis signs and symptoms

A

Flank f=tenderness
Fever
Hypotenstion and tachycardia f the stine is septic

Sevrer loint ot groin pain
Fluctuating in severity
N%V
Urinary urgancy and frequancy
Heamatauria
Oligurina
Fever if its septic

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7
Q

Nephrolithiasis 1st line tests

A
  • Urinanalysis for haematuria
  • Inflamatory markers 0 raised WBC and CRP
  • U &E - riased creaties suggets AKI due to obstruction
    Bone sprofie and urate - elevated calcoum may show yperperparathyroidism

CT urogram fr diagnosing

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8
Q

Nephrolithiasis differenctils

A

Rubtured abdominal aortic anyerism
Apperdicitis
Ectpic pregnancy
Ovarian cyst
Bowel obstruction
Diverticulits

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9
Q

Nephrolithiasis treatment

A

Acute:
* IV fluids and antiemetics
* NSAID, then paracetamol secondary
* Antibiotics if there is an infection present
Surgical:
* Ureteroscopy - ureteeroscope into the ureter and retrieve the stone with intracoporeal lithotripsy
* Extracorporeal shock wave lithotripsy - high energy sound waves to break down the stones fomr outside of the body
* Percutaneous nephrolithotomy - surgical inscision in the bac for intracorporal lithoptripsy
* Uretal stention

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10
Q

Nephrolithiasis monitering

A
  • Increases oral fluids
  • Rediced dietry salt intake
  • Reduce oxalate rich foods for calcium stones - spinach , nutsm tea
  • Reduce intake of urate high stones - kidney, liver, sardines
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11
Q

Acute kidney injury definition

A

sudden decline in kidney function over a few days

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12
Q

Acute kidney injury causes

A

Pre-Renal –
* Sepsis
* Dehydration
* Hemorrhage
* Cardiac failure
* Liver failure
* Renal artery stenosis
Intra-renal –
* Nephrotoxins
* Parenchymal disease etc Multiple myeloma
Post-Renal –
* Ureteric
* Retroperitoneal Fibrosis
* Bilateral renal stones
* Tumors
* Bladder
* Acute Urinary Retention
* Blocked catheter
* Urethral
* Prostatic enlargement
* Renal stones

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13
Q

Acute kidney injury risk factors

A

65 >=
Pre-existing kidney problem
Dehydrated
Blockage in your urinary tract
Sepsis
Immunocompromise
Toxins
Hypovolemia

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14
Q

Acute kidney injury pathophysiology

A

Pre renal -
* Hypofusion due to hypovolemua due to: cardiac faliure, hypoalbuimneria. The lack of blood causes ischemia and damage
Intrinsic -
* Vascular damage - athersclarosis, thrombusus, dissections,
* Glomerular damage - can lead to nephritic syndreom
* Tubulo interstitial due toi necrosis, can be secondary to medications or infectino based
Post renal -
Onstruction - urinary stones, malignayc, strictures

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15
Q

Acute kidney injury key presintations

A
  • Feeling sick
  • Diarrhoea
  • Dehydration
  • Confusion
  • Drowsiness
  • Reduced capillery refill - if hypovolemic cause
  • Tachycardia
  • OLIGAURIA - less weeeeee
  • Postural hypotension

There are two classification systems
* RIFLE - the last 2 are turned into chornic
* You measure creatine and urine output
*
* KDIGO - says tha causes kidney disease is an increases in serum creatine >26.5 in 48 hours,
- An increase in serum creatinine to ≥ 1.5 times baseline within 7 days
- Urine output < 0.5 mL/kg/hr for six hours

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16
Q

Acute kidney injury fist line test

A
  • Serum creatinine test - acute rise
  • Fbc - high ER might siggest vasculitis, serum calcium, phosphate and ruic acid for kidney stones
  • Urineanalysis - blood, nitrates, leukocytes, proteins
  • reanl ultrasound to ook for kidney stones
  • Monitor kidney output
  • Urine and blood cultures to exclude infection
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17
Q

Acute kidney injury treatment

A

Treat the underlying causes -
* Prerenal - correct fluid depletion, treat sepsis with antibiotics
* Renal - refer to nephrology
* Post renal - cathaterise and consider CT KUB

* Stop any nephrotoxis drugs  NSAIDS, ACE inhibitors, gentamcin, amphotecterin 
* Treat hyperkalaema, pulmonary oedema, uraremia and acidaemia 
* Dialysis to remove toxins form the body  Drig over dose -  barbiturate, lithium, alcohol-ethylene glycol, salicylate, theophylline
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18
Q

Acute kidney injury complications

A

Hyperkalaemia!! This is associated with tall peaked T waves, wides QRS, small p waves. To manage give insulin and dextrose to drive the K+ fomr the blood into the cells, gve salbutamol and IV fluids

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19
Q

chronic kidney disease definition

A

Long standing progressive abdormailty of kidney function - a reduction in GFR <60ml/min/173M^2 for longer than 3 months

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20
Q

chronic kidney disease epidemiology

A

6-11% of people have CKD
F>M

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21
Q

chronic kidney disease causes

A
  • Hypertension- the walls thinken to withstand the pressre whhc leads t a narrow lumen, less bloood fow, ischeamia. The ischeami leads to glumerulosclarosis (hardening and scarring) which leads to dimined siltering ability
  • Diabeties - excess glucose sticks to protiens and make it stiff and narrow, it cuases obstruction which leadst o hyerfiltrtoin ang glomerulosclerosis
  • Polyscystc kidney disease
  • Any glomerular disease - IgA nephropathy, wegeners granulomatosis, amyloydosis, nephrotic syndrome
  • Chronic NSAID use
  • SLE
  • Nephrotoxic drugs
  • Meloma
    Enlarged prostate/kidney stone
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22
Q

chronic kidney disease risk factors

A
  • Diabeties,
  • Hypertnsion
  • SLE
  • Female gender
  • Smoking
  • lV hypertrophy
    Family history
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23
Q

chronic kidney disease pathophysiology

A
  • CKD leads to end stage kidney disease
  • The speed of decline depends on the nephropathy and BP control
  • Sine of the nephrons die which leavs a harder job to the other nephrins who need to make up for it, which causes hypertrophy and reduced arterilar resistance
    This increased pressure and strain accelerated the nephron failing
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24
Q

chronic kidney disease signs

A
  • Small kidneys on ultrasoun
  • Pallor
  • Hypertension
  • Peripheral oedema
  • Pleural effusion
  • lV hypertrophy
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25
Q

chronic kidney disease symptoms

A
  • Urinary changes - oligureia, polyurina, protinuria, haematuria, nocturia
  • Non specitfic - tremor, malaise, nausea, hiccpus, legarthy
  • Bone diseases - causes by lack of 25-dehydroxyvitamin D leading to excess PTH to be release to make up for a lack of calcium leading to pseudofractures and pain
  • Anaemia - less EPO, the liver makes hepdacin which the kidneys wxcrete which leads to a build up and reductiong of intestinal iron absorbtion
  • Hyperkaleamia - weakness and paralyis, metabolic acidosis, cardiac arrhythmias
  • Cardiovascualr disease - ureamic pericarditis, hypertension, peripheral vascualr disease
  • Neurologila - confusion, coma, fits
  • Colume overload - dyspnea, oedema
    Sexual dysfunction
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26
Q

chronic kidney disease test

A
  • FBC - aanaemia, creatin and urea, decreased CA2+, rasied phosphate , K+ and renin
  • U&Es
  • Urine and blood cultures - UTI,
  • Urine dip stick - haemtouria and protinaureia suggetss glomerular necrosis
  • Albumin ot creatine ration, protien to creating ration
  • Renal ultrasoud for obstruction
  • Serum biochemistry- U&Es, creatine, bicarbonate
    CT - usefu for diagnosis of retroperitoneal fibrosis and urinary obstruction
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27
Q

chronic kidney disease treatment

A
  • Treat underlying causes - antibiotics, immunosurpressant for vasculitis, metabolic controll in diabetties, stop nephrotoxic drugs, IV fluid for volume depletion, manage blood pressure,
  • Statins
  • Lifestyle - less sodium and potassiom, vitamin d supplement
  • Stop nephrotoxic drugs
  • Treat hyperkalaemia
  • Dialysis
    Kindney transplant
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28
Q

chronic kidney disease complications

A

Hyperkalaemia
Vit d deficancy
Hypertension
Pericarditis
Aneamia
Metabolic acidosis
Oseeoporosis

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29
Q

UTI definition

A

The inflammatory response of the urothelium to bacterial invasion with bacteriuria and pyuria. It is the growth of >10^5 organism/ml of fresh mid-stream urine

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30
Q

UTI epidemiology

A

Women - 20% will have one in their lifetime
Elderly patients
Hospitalized patients
Renal transplant

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31
Q

UTI causes

A

Gram negative
* E Coli (most common)
* Proteus mirablis - renal stones
* Klemsiella pneumonia - hospital catheters
* Pseudomonas aerginosa - underlying pathology

Gram positive:
* Staph saprophyticus - lactose fermenting, catalase positive, coagulase negative - 2nd most common, the sex one for females
* Enterococcus

TB
Catheterisation - incomplete voiding and urine statists

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32
Q

UTI risk factors

A

Female
Sex! No surely not!
Menopause
Catheterisation
Pregnancy n
Diabetes
Urinar tract obstructions
Malformations
Immunosurpression

Asymptomatic - over 65s
Uncomplicated - non pregnant females
Complicated - children, pregnant females, immunocompramised, urosepsis, cataterised patients

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33
Q

UTI pathophysiology

A

Urine is sterile but bacerial which livs normally fine can move up. Often bowl flora.
Lower UTIs are notammly due to an ascending infection - cystitis, urethritis, prostatitis
Epidydimal orchitis is where the testicles and epidimus become swollen and painful due to an infection

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34
Q

UTI signs

A

Pyuria

lower - incontanence, pain on peeinf
Upper - fever and haematuria

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35
Q

UTI symptoms

A

Upper UTI – systemic symptoms
Loin/abdominal pain
Tenderness
Nausea
Vomiting
Fever
Costovertebral angle pain

Lower UTI – HD FUSS
Hematuria
Dysuria
Frequency
Urgency
Suprapubic pain
Smelly urine

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36
Q

UTI tests

A
  • Urine dipstick - blood, proteins, nitrites leukocytes, pH, glucose, ketones
  • Midstream sample - voids the bacteria and get it fresh
  • Supra pubic aspirate
  • Early morning urine - look for TB that has accumulated in the urine
    Microscopy - WBC increase, RBC, bacteria, epithelial cells, cultures
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37
Q

UTI treatment

A
  • If its asymptomatic, then don’t treat
  • Uncomplicated - non pregnant females - give 3 days of antibiotics, increased fluid intake, void post intercourse and improve hygine
  • Complicated - always send culture, 7 day antibiotic course, nitrofurantoin should be avoided in pregnancy and has side effects of N&V, liver problems and weakness.
  • New antibiotics are reserved for the resistant infection- fosfomycin, pivemcillin

1st line - nitrofurantoin (1st trimester preganys only!) trimethoprim (3rd trimester pregnancy only!) or cefalexin

2nd line - ciprofloxacin or co amoxiclav

To prevent, drink fluids, urinate after sex and have good hygine.

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38
Q

pyelonephritis definition

A

Infection of the parenchymal soft tissue of the renal pelvis and upper ureter

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39
Q

pyelonephritis UTI epidemiology

A

Females under over 35
Significant sepsis and system upset

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40
Q

pyelonephritis causes

A

KEEP

Klebsiella
Enterobacter
E coli - most common
Proteus

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41
Q

pyelonephritis risk factorss

A

Structural renal abnormalities -which causes vesicoureteral reflux
Catheterisation
Pregnancy
Diabetes
Immunosuppression
Calcuili

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42
Q

pyelonephritis pathophysiology

A

Infection is normally from bacteria from the aptines own bowel
It can be ascending, or come from eh blood stream or lymphatics
Haematogenous - aureus , candida
Lymphatic - rare

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43
Q

pyelonephritis signs and symptoms

A

Usually unilateral

Triad of loin/flank pain, fever, pyuria
N&V
Costovertebral angle pain
Rigors (chills)

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44
Q

pyelonephritis tests

A

Urine dipstick - nitites, bacterial breakdown produced nities
WBC
Foul smelling urine

Abdominal investigation - tender loin, renal angle tenderness, vag exm -rule out pathology there

Bloods- wBC ESR nd CRP may all be raised
Ultraous to tule out obstruction

Gold standard: MSU with microscopy, culture and sensitivity!

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45
Q

pyelonephritis differential

A

Diverticulitis
Abdomial aortic anyerism
Kisdey stones cystitis
Proastatitis

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46
Q

pyelonephritis treatments

A

Hydration - fluid repkacement
IV antibiotoc - brad spectrum - co amoxilav and gentamicin
If pregnancy use cefalexin
Drai the obstructed kidney
Cathater
Analgesia
7-14 das of antibiotics

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47
Q

pyelonephritis complications

A

Renal absess - no respnse to antibiotics, imaging sows then
Emphsematous pyeloneophritis - gas accumulationin liddues, life threataning, may need nephrectom

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48
Q

cystitis definition, epedemiology and bacterial causes

A

Urinary infection of the bladder

Females

E coli

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49
Q

cystitis risk factros

A

Urinary stasis
Bladder stones
Poor emptying

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50
Q

cystitis key presintations

A

HD FUSS

* Haematuria 
* Dysuria 
* Frequency 
* Urgency 
* Suprapubic pain 
* Smelly urine  Loin tenderness
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51
Q

cystitis key presintaiotiosn

A

HD FUSS

* Haematuria 
* Dysuria 
* Frequency 
* Urgency 
* Suprapubic pain 
* Smelly urine  Loin tenderness
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52
Q

cystitis first line test

A

Microscopy and sensitivoty of MSU - gold standard

Urine dipstick - positive for leuokocytes, blood and nitrates

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53
Q

cystitis treatment

A

1st line - nitrofurantoin (1st trimester pregant only ) trimethoprim (3rd trimester only) or cefalexin

2nd line - ciprofloxacin or co amoxiclav

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54
Q

prostatitis definition

A

Infection of the prostate gland

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55
Q

prostatitis causes

A
  • Acute prostatis - strep faecalis, Ecoli, Chlamydia
    Chornic- strep, faecalis, ecohil or chlamydia, elevated prosteate pressure, pelvic floor myalgia
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56
Q

prostatitis risk factors

A

Sti
Uti
Indwellign cathater
Post biopsy
Increasing age

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57
Q

prostatitis key presintations

A

Systemically unwell
Fever
Malaise
Rigirs
Painful ejaculating
Pelvic pain
Voiding LUTS - streaming poor stream, incomplete emptying, hesitancy, dysuria.

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58
Q

prostatitis tests

A

DRE - prostate is tender and hard from calcification

Blood cultrues
MSU
STI screen
Urine dipstick - posituve or leucoctes and nitries
Trans ureteral ultrasoud

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59
Q

prostatitis differential

A

Cystitis
BPH
Calculi
Prostatic abcess
Malignancy

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60
Q

prostatitis treatmetn

A
  • Acute - gentimicin and co-amoxiclav
  • Second line trumethroprim

Chronic - 4-6 week course of quinooone, ciprofloxacin - alpha blocker - tamsulosin

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61
Q

urethritis definition

A

Uretheral inflamation

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62
Q

Urethritis epidemiology

A

Diagnosed in men at SH clinics
Non conoccocal urethritis is more common

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63
Q

Urethritis cases

A
  • Neisseria gonorrhoea
  • Chlamydia - most common
    Mycoplasma genitalium
  • Trichomonas vaginalis
  • Non-infective:
    Trauma
    Urethral stricture
    Irritation
    Urinary calculi (stones)
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64
Q

Urethritis risk factors

A

Unprotected sex
Male to male sex

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65
Q

Urethritis key presintations

A
  • Asymtomatic
  • Sysutia
  • Discharge and pain
  • Uretheral pain
  • Penile discomfort
  • Skin lesions
    Systemic symptoms
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66
Q

Urethritis test

A
  • Nucleic acid amplification test
  • Microscopy of gram stainesd smears fo fenital secretions
  • Blood cultures
  • Urine dipstic
    Uretheral smear
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67
Q

Urethritis differential

A

Candida balanitis
Epididymitis
Cystitis
Acute prostatitis
Urethral malignancy

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68
Q

Urethritis treatment

A
  • Chlamydia
    ○ Oral azithromycin or 1-week oral doxycycline
    ○ Pregnant – oral erythromycin (14 days) or oral azithromycin
  • Gonorrhoea
    ○ IM ceftriaxone with oral azithromycin
    ○ Partner notification
  • Patient education
    Contact tracing
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69
Q

Epidydimo- orichitis definition

A

Swellling of the epidydimus that can spread to the testes

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70
Q

Epidydimo- orichitis causes

A

STI - chlamydia and gonorrhoea

Utis - klebsiella, ecoli enttterococcus, pseudomonias, staphylococcus
Mumps
Trauma
Elderly

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71
Q

Epidydimo- orichitis risk factors

A

Previous infections
Indwelling catheter
Abrnormality f the urinary tract
Anal intercourse

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72
Q

Epidydimo- orichitis key presintations

A
  • Scrotal pain and swelling
  • Urethritis
  • Uretheral discharge
  • Mumps - eadach and fever
  • Tenderness
    Sweats/fever
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73
Q

Epidydimo- orichitis test

A
  • Nucelic acid amplification test
  • MSU dipstick
  • Ultrasound to rule out abcess
  • Blood cultrues
  • STI screening
    Iretheral smear and swab
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74
Q

Epidydimo- orichitis differntial

A

Testicular torsion
Hydrocele
Trauma
Abcess

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75
Q

Epidydimo- orichitis treatmetn

A
  • Chlamydia
    ○ Oral azithromycin or 1 week oral doxycycline
    ○ Pregnant – oral erythromycin (14 days) or oral azithromycin
  • Gonorrhoea
    ○ IM ceftriaxone with oral azithromycin
    ○ Partner notification
  • UTI
    ○ Oral ciprofloxacin
  • Analgesia – NSAIDs e.g. ibuprofen
  • Partner notification and testing
    Abstinence
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76
Q

define nephrtic and nephrotic syndrome

A
  • Nephritic syndrome means that there is a round of symptoms - haematuria, oliguria, proteinuria, fluid retention
    Nephrotic syndrome means that the person has a goup of symptos which are oedema, protinuria low serum albumin and hypercholesterolaemia
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77
Q

define glomerulonephritis

A
  • Glomerulonephritis - inflammation of the glomeruli and nephrons the consequences of which are:
    * Restricted blood flow leading to increased BP
    * Damage to filtration mechanism to blood and protein enter urine
    * Loss of filtration capacity leading to acute kidney injury
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78
Q

what is used to see if there is bleeding in teh kidnyes

A

red blood cast cells in teh urine!

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79
Q

Nephrotic syndome key presintations

A
  • Periphreal oedema
  • Protinuria more >3g/24 hours
  • Serum albumin less than 25g/l
    Hypercholesterolaemia
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80
Q

Nephrotic syndome additional symptoms

A
  • Frothy urine
  • High cholesterol
    Hypercoagulabilityleading to increased wirk of thrombus
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81
Q

Nephrotic syndome treatment

A
  • Immunsurpression with sterioid (predinisilone)
  • Blood pressure bontroll with ACEi or ARB
  • Diuretics for oedema
    Water and salt restrictinos in diet
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82
Q

Nephrotic syndome types

A
  • Minimal change disease - most common in children, treated with sterioids, its idiopathic
  • Focal segmental glomerulosclarosis - most common in adults
  • Membranous glomerulonephritis - most common glomerulonephritis overall, IgG and complement depositis in the basement membrane. Idiopathic causes, can be secaondary to malinnancy, rhumatoid diseases, drugs, Hep B&C and NSAIDs
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83
Q

Nephritic syndome key presintations

A
  • Haematuria
  • Oliguria
  • Proteinuria
    Fluid retention (oedema)
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84
Q

Nephritic syndome treat,ent

A
  • Immunsurpression with sterioid (predinisilone)
  • Blood pressure bontroll with ACEi or ARB
  • Diuretics for oedema
    Water and salt restrictinos in diet
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85
Q

Nephritic syndome types

A
  • IgA nephropathy - the mos cmoon causes of primary, peak age is 20, histology shows IgA depositis and glomerular mesangial proliferation (bergesrs disease)
  • post streptococcla glomerulonehritis (diffuse proliferative glomerulonephritis) - paitint under 30, 1-3 weeks after strep pyogenes infection (URTI), usually a full recovery.
    Goodpasture’s syndrome - anti GBM antibodies attack the glomerulus and pulmonary basement membranes causing glomerulonephritis and pulmonary haemorrhage - patients present with acute kidney failure and haemoptysis
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86
Q

diiffuse proliferaev glomerulonehritis definition, epidemiology, pathophysiology tests and treatmenr

A

Diffuse proliferative glomerulonephritis

The most common form of lupus nephritis

More common in females
And between 15-45 age

Autoimmune condition from lupus - this is when it’s at stage 4 of the progression

Renal biopsy -

Prednisolone

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87
Q

membranoproliferative glomerulonephritis definition, tests and treatment

A

Autoimmune disease - lupus, sarcoidosis,, Sjogren, cancer (leukaemia, lymphoma) Hep B&C, endocarditis, malaria. It is caused by kidney deposits in the membrane and mesangium.

Not to be confused with membranous glomerulonephritis which is just lupus formed and affects the BM only

Renal biopsy

Prednisolone

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88
Q

Nephrotic syndome calssic triad ofkey presintations

A

There is a classic triad of:
* Low serum albumin
* High urine protein
Oedema

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89
Q

Nephrotic syndome signs and symptoms

A

Oedema
Xanthalsma

Xanthoma
Leukonychia
Shortness of breat

  • Peripheral oedema
  • Facial oedema
  • Frothiness of rine
  • Fatigue
  • Poor appetite
  • Reoccurent infections
    Venous/arterial thrombosis due t hypercoagulabilit
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90
Q

Nephrotic syndome tests

A

Urine dipstick - high protein
Frothy appearance

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91
Q

Nephrotic syndome treatmetn

A
  • Loops diuretic for oedema
  • Ace inhibitors to reduce proinurina
  • Statins to reduce cholesterol
    Anticoagulants if necessary treat the underlying causes - stop causative drugs etc
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92
Q

Nephrotic syndome complications

A
  • Higher risk of thromboembolism due to hypercoagulability
    Hyperlipidaemia - bad for strokes and MI
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93
Q

minimal change disease definiftion

A

Nephrotic syndrome occurs in isolation without any clear underlying conditions

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94
Q

what is teh most common causes of nephrotic syndrome in children

A

minimal change disease

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95
Q

minimal change disease tests

A

Renal biopsy and microspecies will not show any abnormalities, urinalysis will show small molecular weight proteins and hyaline casts

96
Q

minimal change disease treatmetn

A
  • Prednisolone or other corticosteroids very effective but there can be remission
  • Restricted fluid and salt diet
  • Albumin infusion
  • IV furosemide - diuretic to reduce oedema, given IV due to bad absorption because of oedema in stomach
97
Q

Focal segmental glomerulosclerosis definition

A

Focal segmental glomerulosclerosis (FSGS) is a chronic pathological process caused by injury to podocytes in the renal glomeruli. It manifests initially with proteinuria, which progresses to nephrotic syndrome and ultimately to end-stage renal failure

98
Q

Focal segmental glomerulosclerosis causes

A

There can be secondary causes - sickle cell diseases, HIV, renal hyperfiltration, heroin abuse
Genetic aspect

99
Q

Focal segmental glomerulosclerosis risk factors

A

Male
Black
Family history
Heroin abus

100
Q

Focal segmental glomerulosclerosis pathophysiology

A
  • Foot process of podocytes damaged leading to plasma proteins and lipids periating the glomerular filter
    Protein and lipids then get trapped and leads to glomerulosclerosis
101
Q

Focal segmental glomerulosclerosis test

A
  • Protein in urine >3.5g/l
    Kidney biopsy most definitive too looks for damage to podocytes
102
Q

Focal segmental glomerulosclerosis treatment

A
  • Treat cause - for example weight loss can help, antiviral therapy for HIV, heroin detoxification
  • Ace inhibitor or angiotensin ii receptor agonist if ace not tolerated and sodium restriction
  • Consider stattin
  • Furosamide and thazide diuretic for oedema
    Immunosuppressants - prednisolone
103
Q

Membranous nephropathy definition

A

Inflammation of the glomerular basement membrane caused by immune complex deposits.

104
Q

Membranous nephropathy epidemiology

A

One of the most common causes of nephrotic syndrome in adults

105
Q

Membranous nephropathy causes

A
  • mainly idiopathic

Secondary:
* Infections - hep B &C, syphyliss
* NSAIDS, pencillamine
* Systemic lupus ertheamatous
Malignancy

106
Q

Membranous nephropathy risk factors

A
  • Male
  • Over 40n
  • Autoimmune disease
107
Q

Membranous nephropathy pathophysiology

A
  • Autoantibodies target the glomerular basement membrane
  • Complexes build up which causes damage to podocytes and mesangial cells
  • There is a recruitment of inflammatory cells which lead to damage and protein leakage
    A diagnosis of primary MN should only be made after secondary causes have been excluded
108
Q

Membranous nephropathy pathophysiology

A
  • Autoantibodies target the glomerular basement membrane
  • Complexes build up which causes damage to podocytes and mesangial cells
  • There is a recruitment of inflammatory cells which lead to damage and protein leakage
    A diagnosis of primary MN should only be made after secondary causes have been excluded
109
Q

Membranous nephropathy test

A
  • Urinanalysis
  • Urine protien to creatine ration
  • Serum urea
  • Serum creatine
  • Biopsy - thiekcening of glomerular membrane

Looks for hepatitis

110
Q

Membranous nephropathy treatment

A
  • Low protien and salt diet
  • Ace inhibitors if hypotensive
  • Statins if hyperlipidaemia
  • Furosemide if oedema
  • Treat the underlying causes
    If there is high ris pf serious kidney injusry give corticosteroids
111
Q

nephritic syndrome definition

A

Haematuria, mild to moderate proteinuria, hypertension, oliguria and red cell casts in the urine.

112
Q

nephritic syndrome key presintations

A
  • Anaemia due to blood loss
  • Oedema dur to hypoalbinuria
    Hypertension to compensate
113
Q

IgA nephropathy definition

A

IgA depositis in the mesangium which leads to the kidye being attack ed by anti-glycan autoantibodies

114
Q

IgA nephropathy key preintations

A
  • Usually in childhhod or during GI or resp infections
  • Haematuria
  • Proteinuria
  • Hypertensin
  • Oedema
  • Oliguria
  • Uraemia
  • Decrease in GFR
    Henoch-Schonlein Purpura (HSP)
115
Q

IgA nephropathy test

A

Urine analysis - erythrocytosis and proteinuria

gold standard: Kidney biopsy - immunofluorescence shows diffuse mesangial proliferation and extracellular matrix expansion

116
Q

IgA nephropathy treatment

A
  • Observation
  • ACE in inhibitors for hypertension
  • Smoking cessation, low salt diet, weight control, exercise
    If more extreme corticosteroid - prednisolone
117
Q

Post strep glomerulonephritis definition and pathophysiology

A
  • Caused by type 3 hypersensitivity
    Immune delayed consequence of pharyngitis or skin infections caused by streptcoccus pyogenous or beta haemolysitc group A strep
    IgG is deposited in the basement membranes which causes an inflammatory reaction in the glomerulus and deposit of inflammatory cytokines, oxidants and proteases that damage the podocytes
118
Q

Post strep glomerulonephritis epidemiology

A
  • Children
    1-2 weeks are upper resp tract infection
119
Q

Post strep glomerulonephritis key presintations

A
  • There will have been a recent infection
    More common in people under 30
120
Q

Post strep glomerulonephritis test

A
  • Kidney biopsy will show glomeruli are hypercellular
    On immunoflorescent tehr are IgG and IgM depositis
121
Q

Post strep glomerulonephritis treatment

A

Furosomide for hypertension
Antibiotics
Usually they make a full recovery

122
Q

goodpastures syndreom definition

A

Type 2 hypersensitivity reaction - Autoimmune condition where there are anti-GBM autoantibodies which attack the

Maly affects the lungs and the kidneys causeing heamoptysis and haemureia

Collagen 4 is the most common in these organs BM, igG antibpdies bind to the collagen chain and activate the complement system, this si a hypersensitivity type 2 reaction

Lung symptoms normally come first

123
Q

goodpastures syndrome causes

A

nfection
Smoking
Oxidative stress

124
Q

goodpastures syndrome key presintations

A
  • Haematuria and heamoptyisis
    Cough, SOB, nausea, lung crackles

if there is blood in the quatar and blood in teh urin, think goodpastrues!!!!!`

125
Q

goodpastures syndrome testing

A
  • Renal function testing

Biopsy- inflammation of BM
Immunofluorescence - shows prescenc of IgG antibodies

126
Q

goodpastures syndrome treatment

A
  • Oral corticosteroid - high does of prednisilone
  • Prophylactive measures for taking hight levles foo steroids
    If treat eed early prognosis is good, they might however need dalysis as it can lead to renal faliure
127
Q

SLE nephropathydefinition

A

nflamation of the kidney due to systemic lupus erythematous. This is causede by antinucleur antibodies whiuc bind to nucler antigens forming antigen-antibody complexes leadsing to deposits and type 3 hypersensitivity reactions

128
Q

SLE nephropathy pathophysiology

A
  • There are different classes depending on severity
    There can be complication such as thrombosis and embolism
129
Q

SLE nephropathy key presintations

A

Rash, arthralgia, pericarditis, pneumonitis

130
Q

SLE nephropathy tests

A

Low complement factros C3 and C4

biopsy

131
Q

SLE nephropathy treatments

A

mmunosurpressants - prednisilone

132
Q

vasculitis nephropathy definition

A

A systemic illness characterised by the inflaation of blood vessles, the blood vessles occulsion and sebsequent isceamin in the organs and tissues

133
Q

benign prostate hyperplasia definition

A

Proloferation o the musculofiberous glandular tissue of the inner zone of the prostate

134
Q

benign prostate hyperplasia epidemiology

A
  • Men <60
  • Incrases in epithelial and stomal cells in the periuretheral area of the prostate
  • Affects afro carribean ethnicitues more than white men
135
Q

benign prostate hyperplasia risk factors

A

Risk Factors

Age
Castration is protective
Family history

136
Q

benign prostate hyperplasia pathophysiology

A

Pathophysiology

  • PSA prostate specific antigen - serine protease responsivle fr liquification of semsn, there is a small amount of leakadge, it is elevated in UTIs, BPE and prostatitis or CANCER
  • Benign proliferation of the transitional zone, the peripheral layer expansion is prostate cancer normally
  • Men produce less testosterone and more dihydrotestosterone which causes hypertrophy from the prostate cells
  • The prostate will then block the bladder causing dilation, urine statis and UTIs
137
Q

benign prostate hyperplasia key preintations

A

Key presentations

Storage -
* Frequency increases
* Urgancy
* Nuctura
* Urgancy incontinence

Voiding - SHIPP

* Straining 
* Hesitancy 
* Incomplete ememptying 
* Poor intermittant stream 
* Post micuration dribiling
138
Q

benign prostate hyperplasia signs

A

Signs

Bladder stones
Urinary retention
UTIs
Haemataure, painful urination are red flags

Painless haematuria is cancer until proven otherwise!!!

139
Q

benign prostate hyperplasia tests

A

1st line test

  • Internation prostate symptom score
  • Digital prostate exam
  • Urine dipstick
  • Tran rectal ultrasound
  • Biopsy
  • Abdominal exam
  • U&E and renal ulatrason
  • PSA - may be raised
140
Q

benign prostate hyperplasia differential

A

Differential diagnosis

Overracive blader syndrome
Bladder tumour
Bladder stonesj
Trauam
UIT
Prostatitis
Biopsy
Bladder/ prostate cancer

141
Q

benign prostate hyperplasia treatment

A

Treatment

  • Avoid caffeine and alcohol
  • 1st line - selective 1- adrenergic receptor antagonist - oral tamsulosin or alfuzosin- relaxes the smooth muscle of the bladders increase urinary flow rate - risk of postural hypotension so should be taken at night
  • 2nd - 5-a-reductase inhibitors - finasteride, dutasteride, inhibit conversion of testosterone to ore active dihydrotestosterone
  • Catheterisation
  • Bladder training
  • Surgical treatment - transurethral resection of the prostate is the gold standard
  • Bladder neck incision
  • Trans ureteral incision of prostate
142
Q

benign prostate hyperplasia complications

A

Complications

Bladder calculi
UTI
Haematuria
Acute retention

143
Q

prostate cancer pathophysiology

A

Normally are adenocarcinomas arising in the periperal zone - 67% of men over 80 have prostate cancer

  • Adenocarcimoas - most common
  • Transitional cell carcinoas = arise form the transitional zone
  • Small cell prostate cancer - neuroendocrine cells
  • Hey may spread through semial vesivles, bladder and rectum, lymph nodes, to bone brain, liver and lung
  • Can metastatise to bone, lung and adjacent issues

PSA can be done for screeing but itsnt very reliable, 70% of raised PSAs arent cancer

144
Q

prostate cancer risk factros

A

Old age
Obesity
Family history
High fat low fibre diet
Black skin
High testosterone

145
Q

prostate cancer symptoms

A
  • Asymptomatic to stat
  • LUTS symptoms the same as BPH - nocturia, hesitancy, poor stream, post micuration dibilling, obstruction, haematuria,
  • B syptoms - weight loss, loss og apetite, night sweats, anaemia
    Bone pain - metastasis
146
Q

prostate cancer tests

A

PSA raised
biopsy and gradingusing teh gleason score
imagign
scan for mets

147
Q

prostate cancer differentials

A

BPH
Prostatitis
Bladder tumour

148
Q

prostate cancer treatment

A
  • Watchful waiting
  • Radical prostatectomy
  • Radical radiotherapy
  • Hormone therapy - to slow the growth, GnRH agonists, androgen recepotr blockers
  • Metastatic - bilateral orichodectom
  • Palliative care
  • Treat hypercalcaemia
    Bisphosphonate
149
Q

testicular cancer epidemiology and risk factros

A

14-44 age
10% of undescended testis
96% arise form germ cells

Undescended testis
Family history

150
Q

testicular cancer signs and symptoms

A

Hydrocele
Testicular mass

Lump on testical
Testicularpain
Abdo pain
Haematospermia
Cough and dysponea
Back pain

151
Q

testicular cancer tests

A

Ultrasound of testes is the best!!!
Biopsy and histology - seminoma - fried egg like
Serum tumour markers - alpha fetoprotine and beta subunit of human chorionic gonadotrophin, lactate dehydrogenase

CXR and CT to asses tumour staging

152
Q

testicular cancer differentials

A

Testicular torsion
Lymphoma
Hydrocele
Epidydimal cyst

153
Q

testicular cancer treatment

A

Radical orchidectomy via inguinal approach to reduce seeding of the tumours
Radiotherapy - seminomas with metastases
Chemotherapy – more widespread tumours and teratomas
Sperm storage

154
Q

kidney cancer epidemiology

A

Renal cell carcinoma
55 age
#male more than female
Most are picked up accidently

155
Q

kidney cancer risk factros

A

Family history
Smoking
Obesity
Hypertension
CKD
Renal abnormalaties
Reanl faliure and haemodialysis

156
Q

kidney cancers signs and symptoms

A

Abdominal mass
Obstruction

Loin flank pain
Haematuria
Abdominal mass
These are eth classic triad!!

B symptoms - night sweats weight loss, loss of appetite
Fever
Anaemia - EPO linked

157
Q

kisney cancer tests

A

Ultrasoun - benign cyst vs complex cyst vs tuour
CT scan - more sensitice ad will show renal involvemebt
MRI
Blood - FBC, U&Em Calcium
Urinanalysis
Biopsy
Bone scan

158
Q

kidney cancer differential

A

Transitional cell carcinoma
Wilms tuour
Renal onocytoma
Leiomyosarcoma

159
Q

kidney cancer treatment

A
  • It is resistant to traditional chemo and RT
  • Ablation/cryotherapy can be done if the tumour is smaller than 4cm or in pallative settings
  • Localised - radical nephrectomy and lymphonodectomy (taking out the whole kidney and the lymph nodes)
  • Partial nephrectomy (only the tumour is removed) if there is bilateral involvement
  • Radiotherapy
  • Metastatic – biological therapies
    ○ Interluekin-2 and interferon alpha
    ○ mTOR inhibitors - temsirolimus
    ○ Tyrosine Kinase inhibitors - sunitinib, sorafenib
    Monoclonal antibodies – bevacizumab
160
Q

kidney cancer compliccations

A

Paraneoplastic syndromes – production of hormones
EPO – more RBCs 🡪 polycythaemia
PTHrP – hypercalcaemia
ACTH – more cortisol 🡪 Cushing’s

161
Q

bladder cancer risk factors

A

Smoking - main one
Paraplegia
Occupational expose to carcinogens - aromatic amines, rubber industry, beta naphthylamine, benzidine and azo dyes
Exposure to drugs e.g. phenacetin and cyclophosphamide
Chronic inflammation of urinary tracts e.g. schistosomiasis (usually associated with squamous carcinoma), bladder stones or indwelling catheters

162
Q

bladder cancer pathophysiiology

A

Tumour spread - localy to pelvic structures
Lympthaitc - to illiac and paraaortic nodes
Haematogenous

90% urothelial transitional cell carcinaomas!!
Squamous cell carcinoma - UTI and kidney sones
Adenocarcinomas - frequently metastasis

163
Q

bladder cancer key presintations

A

Painless haematuria - think bladder cancer!!!!! (1/5 have a malignancy)
Reoccur ant UTIs or UTI like symptoms - frequency urgency, dysuria but absence if bacteria
LUTS -
Mucusuria
Abdominal mass
B symptoms - weight loss, night sweats, loss of appetite
Voiding irritability

164
Q

bladder cancer tests

A

Cystoscopy and biopsy - diagnostic
Urine dipstick
Urine microscopy
Urinary tumour markers
CT/MRI of pelvis

CT urogram – provides staging and is diagnostic

165
Q

bladder cancer differntial

A

Haemorragic cystitis
Renal cancer
UTI
Uretheral trauam

166
Q

bladder cancer treatmetn

A
  • Non-muscle invading bladder cancer (Ta or T1)
    ○ Transurethral resection of bladder tumour (TURBT)
    § Specimen must include muscle to stage
    ○ Mitomycin C
    ○ BCG
  • Muscle invasion
    ○ Radical cystectomy and conduit/neobladder
    ○ Radical radiotherapy ± chemotherapy
  • Transuretheral resectino of blader - both diagnostic and can be a tratment
  • Intravestical therapy - mitomycin - reduced reoccuranc eof bladder cancer, it is put inot the bladder, left for an hour and then removed. This is an antibiotic but it very cytotoxic.
  • Radical cystoprostectomy - removal of prostate and bladder
    Anterior exteneration - removal pf bladder, urethram ureters, uterus and vagina.
167
Q

Polycystic kidney disease definition

A

Genetic disorder where the kidney becomes surrounded by flid
Multiple cysts gradullay grow and cuases renal enlargement, kidney destruction and reanl faliure

168
Q

Polycystic kidney disease causes

A

Simple - develop over time
Aquires - ckd
Genetic
Syndromic diseases - Tuberous sclarosis
Drugs - lithium

169
Q

Polycystic kidney disease cyst types

A

Difference tyoes
* Simple - benign
* Polycystic - mustiple
* Dysplasia - not formed correctly
* Medullary sponge - dilation of collecting ducts
* Acquired cystic disease

170
Q

Polycystic kidney disease pathophysiilogy

A
  • If genetic there is a predisposition to cyst formation
    Increased abnormal cell hyperproliferation 🡪 loss of planar polarity 🡪 cyst initiation
171
Q

Autosomal dominant PKD cause

A
  • Mutation on PKD1 gene on chromosom 15 - more severe and earlier onset
    Mutaiton on PKD” on chromoxome 4 - less severe and later noset
172
Q

Autosomal dominant PKD pathophysiology

A
  • PKD1 encodes polycystin 1 which is involved in cell-cell and/or cell-matrix interactions – regulates tubular and vascular development in kidneys
  • PKD2 encodes polycystic 2 which functions as a calcium ion channel
    Disruption results in reduced cytoplasmic Ca2+ causes disorientated cell division and cyst formation
173
Q

Autosomal dominant PKD signs

A
  • Hypertension
  • UTI and pyelonephritis
  • Renal failure
  • Sub arachnoid haemorrhage
    Liver cysts
174
Q

Autosomal dominant PKD symptoms

A
  • Loin pain
  • UTI
  • Abdominal dicomfort
  • Noturia
  • Heamaturia
    Renal colit due to clots
175
Q

Autosomal dominant PKD tests

A

Genetic testing for PKD1 and PKD2

Ultrasound – diagnostic if:
With Fx - <30 at least 2 cysts
15-39 years > 3 cysts (uni/bilateral)
40-59 years > 2 cysts (each kidney)
> 60 years > 4 cysts (each kidney)

176
Q

Autosomal dominant PKD differential

A
  • Aquired cysts
  • Autosoma recessive
    Tuberous sclaros
177
Q

Autosomal dominant PKD treatmetn

A
  • Blood pressure controll
  • Laproscopic removal of cysts to help with pain
  • Nephrectomy
    Renal replaceent therapy
178
Q

Autosomal recessive PKD epidiemiology and chomosome causes

A
  • More rare
  • Disease of infancy - cilhdern born with cysts

PKHD1 mutaiton on chromosom 6

179
Q

Autosoma lrecessive PKD key presintations

A
  • Infancy renal cysts and congential hepatic fibrosis
  • Renal faliure before birth leading to low amniotic fluid and potter sequence
    Kidney faliure
180
Q

Autosomal recessive PKD differential

A
  • ADPKD
  • Hydro nephritis
    Renal vein thrombosis
181
Q

autosomal recessive PCKD treatment

A
  • Blood pressure controll
  • Laproscopic removal of cysts to help with pain
  • Nephrectomy
  • Renal replaceent therapy
  • Lver transplant
    Genetic counselling for family
182
Q

chlamydia causes

A

Chlamydia trachomatis - gram negative bacteria

Infect the non sqamous epithelia - urethra, endocervical canal, rectum, pharynx, conjunctiva

In neonates it affects the conjunctiva and sometimes can causes atypical pneumonia

183
Q

chlamydia key presintations of males and females

A

MALES:

* Main sight of infection if urethra 
* Dysuria and ureteral discharge 
* Asymptomatic 
* Empdydimo-orichitis and reactive arthritis complications 
*  high transmission to females 

FEMALES:

* Main infetion sight is endocerviacl canal 
* Non speciful symptos - dischage, menstra irragularity, dysuria
* Asymtpatic 
* High transmission 
* Complications: pelvic inflamatory disease, ectopic preganc, chronic pelvic pain, infertility  Neonatal transmissoin
184
Q

chlamydia firs line tests

A

Nucleic acid amplification test - high sensitivity and specificity

* First void urine 
* Endocervicla swab  Self-collected vaginal swab
185
Q

chlamydia treatments

A

Partner management
Test for other STIs

  • Doxycycline 100mg bd for 7 days or azithromycin (1 dose)
  • Erythromycin 500mg bd for 14 days OR azithromycin in pregnancy
    ○ Doxycycline in pregnancy can cause tooth staining
    Antibiotic resistance not a clinically important problem
186
Q

Gonorrhoea causes

A

Neisseria gonorrhoea - gram negative bacteria

Male more

Infect the non squamous epithelia - urethra, endocervical canal, rectum, pharynx, conjunctiva

187
Q

Gonorrhoea test

A

Near person test - microscopy of genital secretion
Looks at the male urethra and female endocervix
Culture on selective medium to confirm diagnosisn
Sensitivity testing
NAAT

188
Q

Gonorrhoea treatmetn

A

Partner notification
Test for other STI’s
Continuous surveillance of antibiotic sensitivity
Single dose treatment preferred
Aim to cure at least 95% of people at first visit
Current regime – Ceftriaxone IM injection with azithromycin

189
Q

Gonorrhoea symptoms

A

Symptoms in women

an unusual vaginal discharge, which may be thin or watery and green or yellow in colour
pain or a burning sensation when passing urine
pain or tenderness in the lower abdominal area – this is less common
bleeding between periods, heavier periods and bleeding after sex – this is less common

Symptoms in men

an unusual discharge from the tip of the penis, which may be white, yellow or green
pain or a burning sensation when urinating
inflammation (swelling) of the foreskin
pain or tenderness in the testicles – this is rare

190
Q

syphellis definition and epidemiology

A

Treponema pallidum sub species - spiral gram negative bacteria

Early infectious syphilis (within 2 years of infection)
Primary, Secondary and Early Latent
Late syphilis (over 2 years since infection)
Late latent, CNS, gummatous

Male
High risk in male to male intercourse

191
Q

syphellis stages

A
  • Incubation is 9-90 days
    • Musly macule/papule hich is hard clean mased and non tender ulcer
    • Primary chancre – 95% genital skin, also nipples, mouth
    • ANY GENITAL ULCER IS SYMPHYLIS UNTILL PROVEN OTHERWISE
    • Secondary - 6-8 months afer infection there is a rash on limbsm pamls and soles, chest, neck and face. Ther is also malaise, lymphadenopathy , alopecia, bone pain, hepatitis, nephrotic syndrome, deafness, meningitis and hepatosplenomegaly
    • ther is then latent stage - an asymptomatic phase
      tertiary stage - affects teh nercous system and ther eis granulomatous on skin bone and internal organs
192
Q

syphellis tests

A

Near person test - microscopy of genital secretion
Looks at the male urethra and female endocervix
Culture on selective medium to confirm diagnosisn
Sensitivity testing
NAAT

Early moist lesions
Genital ulcers
SEROLOGY- look for antibodies against T pallidum antigens

*  there are primary sceeenign tests and then tests done in more detail for those which test postive 
* Treponema pallidum particle agglutination test (TPPA)
193
Q

syphyllus treatmetn

A
  • Penicillin IM
    Efficant follow up and partner notification
194
Q

Varocele definition

A

Abnormla dilation of testicular veins in the pampiform venous plexus cuases by venous reflux

195
Q

Varocele epidemiology

A

Left side more commonly affected, incedence increases after pubity,
Associated wth sub fertility

196
Q

Varocele causes

A

ncreased reflux form renal vein
Lack of effective vaves between testicular and renal veins

197
Q

Varocele signs and symtoms

A

Visable as distended scorla blood vessle that feel like a bag of worms

Sull ache
Scroal heaviness

198
Q

Varocele test

A

Venography
Colour duplex ultrasoud

199
Q

Varocele differential

A

Secondary to pathalogical process - kidney timous and retroperitona tumours

200
Q

Varocele treatmetn

A

surgery is there is pain, infertikity ot testicualr atrophy

201
Q

hydrocele definition

A

Abnormal colleciton of fluid within the tunica vaginalis

202
Q

hydrocele causes

A

Primary - more common and larger, younger men, patent processus vaginalus
Secondayr - older boys and men, secondary to a tumour, trauma, infection, TB, torsion or general oedema

203
Q

hydocele pathophysiology

A

Overproduction oif fluid in the tunica vaginalis
Comunicating - processus vaginalus falied to close allowing peritoneal fluid to communicate freelt with scrotal portion

204
Q

hydocele signs

A

Scrotal enlargement with non-tender, smooth cyctic sweli g
Testis is palpable normally
Lies anterior to and below the testis, will transilluminate

205
Q

hydocele first line test

A

Scrotal ultrasound
Serum AFP and HCG to look for malignant teratomas or other germ cell tumour

206
Q

hydocele differential

A

Testicular torsion
Strangulated hernia

207
Q

hydocele treatmetn

A

esolve spontaneously
Many from infancy resolve by 2
Therapeutic aspiration or surgical removal

208
Q

epidysimal cyst definition

A

Smooth extratesticular sperical cyst in the head of the epidermis

209
Q

epidydimal cysts pathophysiology

A

Clear and milky fluid
Lies benind the testis

210
Q

epidydimal cyst sins and sytoms

A

Lump
Translaminar
Testis palpable separately from the cyst

Painful if large

211
Q

epidydaml cysts test

A

Scrotal ultrasound

212
Q

epidydimal cysts differntial

A
  • Spermatocele fluid and sperm filled cyst between epidermis
  • Hydrocele
    Varicocele
213
Q

epidydimal cyst treatmtne

A

Normally left
Surgical excision if painful

214
Q

testicular torsion definition and epidemiology

A

Commmon urilogical emergcanc
Most commin in post pubertal boys but can be in all ages
Left side more commonly affected

215
Q

testicular torions causes

A

Adlescents and neonated - bell clapper deformitio - - testes is inadaquatly connected to the scrotum which allowsit to move freely on an axis and is more suseptabe to twisting

Adults - malignancy

There is a slight genetic predisposition

216
Q

testicualr torsion pathohysiology

A

Twising of the soermatic cord which cuts off blood supply to the testes
Leads to ischeami, infarction and potenital loss of testis
Germ cells are most suseptable to ischeamia

217
Q

testicular torsion sigs and symptoms

A

Unilateral pain
High riding testicle
Absent cremasteric reflex

Sudden onset testicular pain - makes walking difficult
Inflamed testicle
Abdo pain
N&V

218
Q

testicular torsion test

A

Duplx ultrasoudn
Urinanalysis

219
Q

testicular torsion differntial

A

Epididymo- orchitis
Hydrocele
Idiopathic scrotal oedema

220
Q

testicualr torsion treatmetn

A

Sugery within 6 hours,
Orchidectomy and bilateral fixation

221
Q

storage LUTS

A

Urgency

frequency

Nocturia

Urge incontinence

222
Q

voiding LUTS

A

Hesitancy

Intermittency

Straining

Terminal dribbiling

Incomplete emptying

Haematuria

Dysuria

223
Q

voiding LUT causes

A

Benign prostatic hyperplasia - most common

Drugs with antimuscaneric effects

Diabetic automonim neuropathy of bladder

Uretheral stricture and phumosis - constricion of the foreskin

Cancer of the prostate, bladder or rectum

224
Q

storage LUT causes

A

UTI

Bladder calculi

Urotheleal carcinoma

Overreactive bladder

225
Q

history questions to ask about LUTS

A

Fluid intake and urine appearance
volume daily
what they’re drinking (look out for tea, coffee and other caffeine containing drinks)
urinary appearance - colour, frothiness, cloudiness, any changes
timing of fluid consumption - especially late evening

Drugs:
diuretics
herbal formulas
illicit drugs - especially ketamine
antidepressants
Broncho dilators
Antihistamines

Co-morbidities
previous surgery’s
previous trauma
neurological disorders
cardo- resp diseases - heart failure
Diabetes poorly controlled

226
Q

what is teh most comon causes of UTIS cenraly and teh most common causes of urethritis

A

UTI - ecoli
urethritis - chlaymidia

227
Q

what will a urine dipstick test show for UTIs

A

Urine dipstick test +leukocytes and + nitrites

228
Q

what does cola coulerd urine mean in kidnye disease

A

Rhabdomyolysis- dangersou muscle breakdown as a result of kidney disease

229
Q

what is teh treatment for TB

A

2 antibiotics (isoniazid and rifampicin) for 6 months.
2 additional antibiotics (pyrazinamide and ethambutol) for the first 2 months of the 6-month treatment period.

230
Q

what are the risk factors and epidemiology fot IgA nephritic syndrome

A

16-35
Asain/white/native american
HIV (becuass of reoccurent infections)

231
Q

what does RIFLE stand for

A

risk injury, faliure, loss, end stage renal faliure

232
Q

what is thr risk criteria in rifle

A

creatinine increased by x1.5
UO <0.5ml/kg/h for 6 hours

233
Q

what is teh injury criteria in RIFLE

A

creatinine increased by x2
UO <0.5ml/kg/h for 12 hours

234
Q

what is the faliure criteria in RIFLE

A

creatinine increased by x3 (or greater than 4mg/dl)
UO <0.3ml/kg/h for 12 hours

235
Q

what does the lloss stand for in RIFLE

A

complete loss f reneal function for longer than 4 weeks

236
Q

what are some nephrotoxic drugs

A

antibiotics, NSIADS, Ace inhibitors