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causes of signs > Urinalysis > Flashcards

Urinalysis Flashcards

1
Q

Colour and turbidity

A

Normal fresh urine clear, varies in colour.
Phosphates and urate precipitation can= cloudy when left to stand in normal urine.
Cloudy fresh urine usually due to leucocytes (pyuria), often with bacteria.
Strong fishy smell- infection.

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2
Q

24 hour urine volume

A

Oliguria
Polyuria
In critically ill measure hourly urine flow to indicate organ perfusion.

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3
Q

Uses of urinalysis

A
  • screening- random eg DM, asymptomatic bacteruria. Selective eg antenatal care, HTN.
  • diagnosis- primary renal disease eg glomerulonephritis, secondary eg becaterial endocarditis, non renal eg DM.
  • monitoring- disease progression eg diabetic nephropathy, drug toxicity eg gold therapy, drug compliance eg rifampicin, illicit drug use eg opioids.
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4
Q

Urine dip specific gravity

A

Reflects urine solute (ion) conc.
High- when kidneys actively reabsorb water eg fluid depletion or renal failure due to reduced perfusion.
Low- failure to conc urine.

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5
Q

Urine dip pH

A

Normal 4.5-8. Usually under 7 (5.5-6.5 due to metabolic activity).
In renal tubular acidosis pH never falls under 5,3 despite acidaemia.
Over 7- metabolic alkalosis. Urease spitting organism infection. Stag horn canaliculi.
Acidic- diet, uric acid canaliculi.
Usually reflects blood pH.

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6
Q

Urine dip glucose

A

Small amounts may be normal.
Glucosuria if over 10mmol/L renal threshold.
Reacts with glucose oxidase on stick. DM screen.
High- DM, pregnancy, sepsis, renal tubular damage.

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7
Q

Urine dip ketones

A

Specific for acetoacetate

High- DKA, starvation, alcohol, very low carb diets. Metabolic acidosis with increased anion gap. Pregnancy.

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8
Q

Urine dip protein (mostly albumin)

A

Significant if above trace (300mg/L).
High- nephrotic syndrome, DM, HTN, pregnancy.
Over 2g/day suggests glomerular disease or overflow abnormal
protein eg multiple myeloma.

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9
Q

Urine dip blood

A

Not differentiate between Hb and Mb. Free Hb/Mb=filed change while intact RBC are broken down on contact and release local Hb= a dot (which coalesce over 250 RBC/ml).
Haemoglobinuria- lysis RBCs, especially present in dilute urine.
UTI (pyelonephritis), menstruation, bladder CA (painless, visible), nephritis, polycystic kidney, catheter trauma, drug eg NSAIDs/furosemide.

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10
Q

Urine dip bilirubin and urobilinogen

A

-Bilirubin not normally present.
Unconjugated bilirubin insoluble.
High conjugated- liver disease or BD obstruction. So obstructive jaundice.
-Urobilinogen up to 33umol/L normal.
High- haemolytic or hepatocellular disease. So pre hepatic jaundice.
Associated with elevated nitrite.

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11
Q

Urine dip leucocyte esterase produced by neutrophils

A

Indicates leucocytes in urine (pyuria)- UTI, inflammation, stone disease, urothelial CA. Vaginal discharge.

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12
Q

Urine dip nitrite

A

Most gram neg (some gram pos) reduce urinary nitrate to nitrite. Detected when large numbers of bacteria.
High- bacteruria so UTI, high protein meal.
Low- not exclude bacteruria.
Sensitive to air exposure- can give false positive.

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13
Q

Urine dip erythrocytes

A

Haematuria- confirmed by micsrcopy of re suspended sediment following centrifuge. Glomerulonephritis. Renal, ureteric, or bladder trauma or tumour.

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14
Q

Urine biochem and serology

A

Urea/creatinine
Creatinine clearance
EGFR
Plasma electrolytes (K, bicarb, Ca, urate)
Osmolality
ALP and PTH
Antinuclear factor and antneutrophil cytoplasmic Abs (ANCA) for lupus or vasculitis affecting the kidney.

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15
Q

Kidney

A

LHS T11-L2
RHS T12-L3
Retroperitoneal
Function REEM: regulation ECF, excretion waste, endocrine synthesis (EPO, renin, PG), metabolism (vitD, insulin, PTH, calcitonin).
Controls volume, osmolarity, pH, waste.
GFR 180L/d filtered= 125ml/min. 1.5L urine per day.
22% resting CO.

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16
Q

Body fluid

A

Average 42L total
ICF cytosol 28L
ECF 14L- interstitial 11, plasma 3, lymph, other (transcellular, synovial, intestinal, CSF, sweat, urine, serous)

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17
Q

Water

A

Osmolality- solute per Kg solvent

Osmolarity- osmoles/L (NaCl 2 osmolar per L)

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18
Q

PCT

A

Absorbs most Na, water, K, HCO3
Absorbs all glucose, aa.
Na/glucose symport (SGLUT 2 Na, 1 glucose), Na/H antiport, Na/aa contransport, Na/Pi, AQP.
Simple cuboidal with BB.

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19
Q

Loop henle

A

Create gradient of increasing osmolarity in medulla by counter current multiplication.
Allow concentration of urine.
Pars recta, thin descending and ascending limbs, thick ascending limb.
Thin descending limb- simple squamous no AT. Water osmosis reabsoprtion, no NaCl reabsorption.
Thin ascending- Passive Na reabsorption.
Thick ascending- simple cuboidal no BB. Yes AT. Impermeable to water. NCCK, ROMK.
NCCK symport.
So hypoosmotic leaving loop.

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20
Q

DCT

A 
Secretes H+
Variable reabsorption Na, Cl, water. 
RAS control Na reabsoprtion. 
Large lumen, lot mito, no BB. 
Early DCT NaCl symport.
Late DCT eNaC. 
Active Na reabsoprtion results in dilution. 
Low water permeability, depends on ADH AQP2. 
Major Ca reabsorption NCX.
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21
Q

CD

A

Passes through high osmolarity medulla.
Water leaves via aquaporins? ADH control.
Large irregular lumen.
Late DCT and CD eNaC.
Principle cells eNaC Na reabsorption.
A-IC cells secrete H+
B-IC cells secrete HCO3. Both actively reabsorb Cl.
Urea reabsoprtion in medullary CD, not cortical.

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22
Q

US imaging

A

XR renal stones, not diagnostic.
IVU contrast XR for collecting system.
US for flow in kidneys and bladder.
CT for stones, tumour, trauma, infection.
MRI soft tissue and angiogram
Nuclear medicine for renal function and obstruction.

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23
Q

Renal corpuscle= bowmans+ glomerulus

A

Vascular pole afferent and efferent arterioles.
Urinary pole bowmans capsule and space.
Bowmans capsule parietal is simple sqaumous.
Filtration barrier= fenstrated capillary endothelium +visceral bowmans capsule (podocytes). Shared bm. Filtration slits.
3 forces in filtering- capillary HP, bowmans HP, capillary vs tubule oncotic pressure.
Autoregulation myogenic AA and EA tone. Increase BP= AA constriction to maintain GFR.
Also TG feedback- MD cells sense NaCl in DCT= reduce GFR if high NaCl (adenosine dilation EA) or increase GFR (PG dilation AA).

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24
Q

Juxtaglomerular apparatus

A

Macula densa of DCT
JG cells of afferent arteriole
Extraglomerular mesangial/lacis cells

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25
Q

Renal BS

A

Renal A
5 segmental As
Interlobar As
Arcuate A
Interlobular A
Afferent arteriole (wider than efferent)= HP forces out water, salt, glucose, urea. NOT cells and PP.
Efferent arteriole to peritubular capillaries or vasa recta if JM nephron.
Only 20% renal A blood is filtered to nephron.

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26
Q

Nephron secretion

A

K, H, NH4, creatinine, urea, hormones, drugs.

Organic cation secretion PCT by H/OC exchange.

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27
Q

GFR

A

Normal male 115-125ml/min. Female 90-100ml/min.
Calculate using creatinine or inulin as are freely filtered but not secreted or metabolised.
GFR= (conc in urine x urine flow) / plasma conc.
also eGFR based on age. Mass, serum creatinine.
T1/2= (0.693 x Vd)/ CL
CL rate usually proportional to plasma conc= linear PK.

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28
Q

Renal CL

A 
More lipohpillic drug= easy diffusion back into plasma. But partition into fat= less plasma conc. 
More hydrophillic (charged)= less easy leave lumen, more likely urine excretion. 
PP binding= less glomerular excretion or removal by OATs and OCTs. 
Tissue protein binding also= less CL as less plasma conc. 
high Vd= liptophillic leaves plasma, so less kidney excretion. 
Low Vd= charged, confined to plasma so more kidney excretion. 
In acid urine, weak acid anions protonated= neutral= lipophilic. 
In alkaline urine more are excreted.
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29
Q

Hepatic CL

A

PI and PII enzymes increase ionic charge on xenobiotics so reduces lipophilicty.

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30
Q

HRH

A

Hepatic disease- less metabolism so less renal CL. Less PP so increase renal CL.
Heart- reduce CO= reduce GFR.
Renal disease- reduced CL.

31
Q

BP control

A

BaroRs carotid sinus and aortic arch.
- ST control: Stretch= signal to medulla= vasodilation and reduce HR= reduce maBP.
-LT control: neurohormonal. RAS, SNS, ADH, ANP.
Low pressure baroRs= increase SNS and ADH= water uptake.
Aldosterone= DCT and CD eNAC.
ADH= CD AQP2.
Increase renal A BP= reduce NaH number and Na/K ATPase activity= natriuresis and duiresis.
ANP- increase Na excretion, reduce aldosterone and ADH and constriction.
PG an ddopamine vasodilation.

32
Q

RAS

A

Low NaCl to DCT, low AA perfusion pressure, and SNS stimulation all signal to JGA sm= renin release.
Renin- angiotensinogen to angI
ACE- angI to angII. Also bradykinin breakdown to peptide fragments.
AngII- vasoconstriction, Na reabsorption (PCT NHE), aldosterone release (activate enac and Na/K ATPase), hypothalamic ADH release (constriction, AQP2, NCCK), SNS increase na (constriction, NHE and N/K activation, more renin).

33
Q

HyperK over 5M

A

Causes-
-increase intake- diet, IV dose
-decrease excretion- A/CKI, ACEi, K sparing duiretic, addisons.
-internal shifts- DKS, cell lysis, metabolic acidosis, exercise.
Consequences-
Arrhythmia, HB (more fast Na channels inactive).
Paralytic ileus.
Acidosis.
ECG- high T, long PR, STD, no P, wide QRS, VF.
Tx- IV Ca gluconate, glucose+insulin, neb salbutamol, dialysis. LT- tx cause, reduce intake, dialysis, K binding resin.

34
Q

HypoK under 3.5M

A

Causes-
-external balance- increase GI or renal loss.
-internal balance- K to ICF eg metabolic alkalosis.
Consequences-
Arrhythmia (more active Na channels)
Paralytic ileus
NMJ muscle weakness
Nephrogenic DI as unresponsive to ADH
ECG- low T, high U, low ST.
Tx- oral/IV K, treat cause, if low MC then K spraing duiretic.

35
Q

Acid base balance

A

Alklaemia- low free Ca, parasthesia and tetany.
Acidaemia- high plasma K, protein denatured.
HCO3 (kidneys): pCO2 (resp) ratio determines plasma pH.
Central chemoRs detect pCO2, slow response.
Peripheral detect pCO2 and pH, fast response, smaller effect.
respiratory change compensated by kidney (increase HCO3 reabsorption PCT via NHE and can make new via alpha KG), metabolic by ventilation.
Anion gap= difference between Na + K and Cl +HCO3. Increases if other anions replace HCO3.

36
Q

ADH

A

Stimulates AQP2 insertion to CD luminal surface= more water reabsorption.
Also increase urea reabsorption CD.
Low plasma ADH= diuresis (DI)
High eg SIADH= anti diuresis

37
Q

Thiazide diuretics eg bendroflumethazide

A

Block NaCl contransport in early DCT. Less potent than loops.
1st line antiHTN. Use in elderly, IHD.
AE- hypoK, gout, reduced glucose tolerance especially if with BB, increase LDL and TG, erectile dysfunction.
NOT WORK in renal failure.
Set low dose.
Activates RAS so may need ACEi too.
Increase Ca reabsorption unlike loop.
DDI- digoxin, BB, steroids, carbamazepine.

38
Q

Loop diuretics eg furosemide.

A

Block NCCK symport in thick ascending limb by binding Cl site.
Very potent as lot Na reabsorption here.
Concurrent Ca and Mg excretion.
Less used in HTN, more in HF or oedema.
AE- hypovolaemia, uric acid high, glucose intolerance, high LDL, hypoK. Furosemide ototoxicity. Bumetanide myalgia.
DDI- aminoglycosides can= oto and nephrotoxicity.

39
Q

K sparing diuretic eg amiloride

A

Block eNAC in late DT and CD. Reduce K loss. Mild affect.
Usually combine with K losing diuretic eg loop or thiazide.
AE- hyperK especially with ACEi, K supplement, or renal impairment.

40
Q

K sparing aldosterone antagonist eg spironolactone

A

Competitive inhibition aldosterone R reduces eNAC reabsorption. Also reduce Na/K APTase activity. Mild effect.
Best for HTN due to hyperalodsteronism eg conns.
1st line ascites and oedema in cirrhosis.
Use with loops in HF.
Add on if HTN not controlled by ACEi, CCB, thiazide.
AE- hyperK especially with ACEi, K supplement, or renal impairment.
Androgenic x relativity. Painful gynaecomastia.

41
Q

Osmotic diuretics eg mannitol

A

Increase filtrate osmolairty throughout nephron.
IV for cerebral oedema.
Not reabsorbed itself.

42
Q

Carbonic anhydrase inhibitor eg acetazolamide

A

Inhibit CA in PCT reduced Na and HCO3 reabsorption. Excretion Na, K, PO3.
AE- metabolic acidosis as HCO3 loss, hypoK.
Used in glaucoma.

43
Q

Urolithiasis= stones in UT.

A

-Kidney stones=solid material formed in kidneys from urine minerals. More in men except struvite.
Stag horn in minor calices- usually struvite.
Non stag horn calyceal or plevic.
99% Ca stones- Ca oxalate, CaP, uric acid, struvite (urease pos infection)
1% other eg cysteine, drug, ammonium.
Urine supersaturation with minerals.
-lodge commonly-
Ureteropelvic junction, x pelvic brim at common iliac bifurcation, ureterovesicular junction.

44
Q

CA homeostasis

A

-PTH=increase serum Ca by- more osteoclast activity, more intestine absorption, more active vitD synthesis, more tubular reabsoprtion, more P excretion.
-Vit D= increase CA absorption in gut, increase calcification and resorption in bone.
-calcitonin from thyroid C cells= reduce serum Ca by- inhibit osteoclast, increase renal excretion Ca and P.
HyperCa bones, stones, moans, groans.

45
Q

Renal stones px

A 
Often asymptomatic 
Renal colic felt along L1 root distribution. 
Dulla che loins if in kidney
Recurrent UTI
Haematuria
Renal failure
UT obstruction
46
Q

Renal stones investigations

A

MSU for RBC, casts, crystals, culture.
Serum for urea, creatinine, electrolytes, Ca.
Abdo XR- most radio opaque, uric acid stones radiolucent.
CT.
Serve urine- can pass under 5mm. Over 7mm surgery.

47
Q

Renal stone complications

A

Acute pyelonephritis, maybe with gram neg septicaemia.
Pressure necrosis of renal parenchyma.
Urinary obstruction and hydronephrisis.
Ulcer through wall of collecting system.

48
Q

Renal stone tx

A 
Analgesia
Uteroscopy 
Percutanaeous nephrolithotomy 
Extra corporeal shock wave lithotripsy 
-prevention- 
Hydration, thiazide, K citrate to alklalinise urine (prevents Ca oxalate but can cause CaP).
49
Q

UTI RFs

A

-Short urethra- female
-Obstruction- prostate, pregnancy, stones, tumour.
-Neuro- incomplete emptying.
PUJ calculi
Ureter calculi, CA, retroperitoneal fibrosis
Bladder neuropathic
VUJ calculi
Bladder neck hypertrophy
Prostate CA or BPH
Urethral stricture
-Reflux- ascending infection from bladder, especially in kids.

50
Q

UTI bacterial VFs

A

Fimbriae attach epithelium
Haemolysins damage renal membranes
Urease breaks down urea
K Ag allows PS capsule production

51
Q

UTI common pathogens ????

A 
Gram neg coliforms eg ecoli
Proteus sp
Enterococci
Coagulase neg staph
Pseudomonas
52
Q

UTI clinical syndromes

A

-LUT-
Cystitis- frequency, dysuria, pyuria, haematuria.
Prostatitis- fever, dysuria, frequency, low back pain.
-UUT-
Acute pyelonephritis- fever, loin pain and cystitis symptoms.
Chronic interstitial nehpritis- CI
-asymptomatic bacteruira- Pregnancy
-septacaemia maybe shock- UTI most common source of gram neg sepsis.

53
Q

UTI S+S

A 
-LUT cystitis-
Dysuria
Frequency
Urgency
Low grade fever
-UUT pyelonephritis-
Fever
Loin pain, often unilateral, poorly localised. 
Maybe dysruia and frequency
54
Q

Complicated UTI

When factors predispose to persistent infection, recurrence, or treament failure.

A

Abnormal UT-catheter, bladder reflux.
Virulent organism- Sa
Impaired host defence- badly controlled DM, immunosuppression.
Impaired renal function.
Children, men and pregnancy women usually count as complicated.
Always urine culture.
If uncomplicated- may not need urine culture.

55
Q

Urine sample

A 
MSU
Clean catch 
Collection bag
Catheter sample 
Supra pubic aspiration
Transport- 4 degrees, boric acid. 
Look for turbidity (WBC)
Urine dip- leucocyte esterase, nitrite. Possibly haematuria and proteinuria.
56
Q

Urine dip use in UTI

A

-useful for exclusion in-
Kids under 3, men with mild symptoms, elderly.
-NOT useful in-
Acute uncomplicated UTI in women.
Men with typical or severe symptoms.
Catherised.
Elderly w/o features of infection as asymptomatic bacteruria common. No risk increase morbidity or mortality. Only act in pregnancy and urological surgery,

57
Q

Other urine tests

A

Microscopy
Lab screeinging- WBC, RBC, bacteria, casts
Culture- and sensitivity testing.

58
Q

UTI tx

A

-Hydration
-Address underlying disorders
-3 day course for uncomplicated. Oral trimethoprim or nitrofurantoin.
-5-7 day for complicated LUTI eg pregnancy, male, underlying disorder. Trimethoprim, nitrofurantoin or cephalexin can be used depending on susceptibility. NOT amoxicillin as lot resistance.
Post tx cultures in kids and pregnancy.
-pyelonephritis or septacaemia- 14 day course. NOT nitrofurantoin as no systemic activity. Co amoxiclav, ciprofloxacin, gentamicin (nephrotoxic, IV only). Maybe IV initally.
-prophylaxis if over 3 episodes in 1 year and no treatable underlying condition. Trimethoprim or nitrofurantoin sungle nightly dose. Document breakthrough infection.
Only tx positive catheter specimen if systemically unwell. Do change/remove catheter.

59
Q

Bladder neurology

A

Micturition PNS (s2,3,4 pelvic Ns)= detrusor contract.
SNS form storage reflex= detrusor relaxation. And internal sphincter contraction.
EUS and levator ani somatic supply pudendal N (s2,3,4).
-LMN lesion= low detrusor pressure. So large residual urine, maybe overflow incontinence. Reduced peri anal sensation and tone, relaxed EUS.
-UMN lesion- SC reflex control only. Constant high pressure detrusor contractions, poor coordination with sphincters which also contract more. Risk retrograde urine.

60
Q

Urinary incontinence

A

Detrusor- hyper contraction, fibrosis so cant distend, or over distension.
Weak plevic floor muscles.
-stress UI
-urge UI- inolvuntary leak with/followed by urgency.
-mixed UI- involuntary leak with urgency and exertion.
-overflow UI
Lifestyle mx- fluid intake, weight loss, smoking, caffeine, constipation, timed voiding.
Tx- indwelling catheter, sheat, pad, pelvic floor exercise.
Fluoxetine na and 5HT uptake inhibition- enhance EUS during filling.
Tapes, suspension, sling surgery females.
Artificial sphincter and sling males.
Anticholinergics
Beta 3 agonist increase storage capacity.
Botulinum toxin.

61
Q

Glomerular pathology

A

-filter blockage, renal failure, low eGFR- NEPHRITIC syndrome:
Haematuria, HTN, renal failure.
Classically post strep in kids.
Other signs- rapid onset, Liguria, some oedema genralised, sometimes proteinuria, raised creatinine and RBC casts, high JVP.
Biopsy for diagnosis.
-filter leak- NEPHROTIC syndrome:
Proteinuria, oedema, hypoalbuminaemia, hyperlipidaemia.
Insidious onset.
Pathognomonic of glomerular disease.
Biopsy for diagnosis.
Other signs- muehrckes bands, xanthlasma, fat bodies in urine, DVT.

62
Q

Nephrotic syndrome

A

-Podocyte or subepithelial injury. Loss foot processes.
-Primary causes-
minimal change glomerulonephritis podocyte effacement.
Focal segment glomerulosclerosis scarring.
Membranous glomerulonephritis most common as adults- immune complex deposits, AI, can be secondary eg to lymphoma. Thick capill loops and spiky glomerulus due to IgG deposition.
-secondary-
DM- progressive proteinuria, macrovascular damage, mesangial sclerosis, bm thickening.
Amyloidosis

63
Q

Nephritic syndrome

A

-nephritic syndrome-
endothelial damage=thrombus.
Or glomerular blockage= reduce GFR, renal failure.
Goodpasture anti GBM Ab to collagen IV, acute onset- IgG deposition, glomerular burst, fibrin.
Vasculitis- ANCA Ab activates neutrophils= inflammatory damage. Segmental bm necrosis, inflammatory cell crescent.
Vasculitis extra renal manifestations eg lung cavities.
-haematuria-
IgA nephropathy MOST COMMON. Infection related. Mesangial damage by IgA deposition. Often leads to renal failure.
hereditary neuropathy: alports (abnormal collagen IV X linked, deafness, often renal fail), thin GBM nephropathy (benign haematuria).

64
Q

Prostate CA

A

Black more than white more than asian.
-symptoms-
Asymptomatic, urianary storage/voiding problems, benign enlargement of prostate/bladder overactivity, bone pain. Haematuria if very advanced.
-diagnosis-
DRE, serum PSA, biopsy, resection, MRI, bone scan.
-localised CA tx-
Surveillance, prostatectomy, radiotherapy.
-mets tx-
Hormones (castration, LHRH agonist), palliative radiotherapy/bisphosphonates/ chemo.

65
Q

Haematuria

A

Visible
Invisible- symptomatic or asymptomatic.
-differentials- UT CA, stones, infection, inflammation, BPH, nephritic syndrome.
-signs- BP, mass, varicocoele, leg swelling, DRE.
-investigation- bloods, urine culture and cytology, cytoscopy, US.
Schistosomiasis and occupational bladder CA risk.
Smoking, obesity and dialysis renal cell carcinoma risk.
Transitional cell carcinoma upper UT often spread to bladder.

66
Q

Kidney disease signs

A

OFTEN ASYMPTOMATIC and opportunistically picked up or missed.
HyperK if filtration impaired
Na overload paralleled by water overload so Na conc remains same but pulmonary and peripheral oedema and HTN.
Acidosis with kussmauls
Fatigue
Uraemia syndrome if very severe failure

67
Q

Impaired tubular function signs

A

Frequency
Nocturia as cant concentrate urine at night
Acidosis
Glycosuria with normal blood glucose.

68
Q

Renal hormone problem signs

A

Metabolic bone disease as cant activate vitD by hydroxylation.
Anaemia as less EPO
HTN as increase renin.

69
Q

AKI screening indications

A 
HTN
Heart disease
DM
UT obstruction 
Systemic disease (myeloma, SLE, other AI)
70
Q

Microscopic haematuria
Very common 22%
If over 45yo require cystoscopy

A 
UTI most common 
Polycystic kidneys
Renal stones 
Renal/bladder tumour
AVM
Kidney/glomerular disease
71
Q

Macroscopic haematuria

A

Brown or smoky in glomerular disease, and mixes in so occurs throughout stream. Usually painless. Most common is IgA nephropathy after URTI. Dysmorphic RBCs and red cell casts present.
Clots- more likely from bladder or tumour
If clears as stream continues- lower UT issue
At end stream- bladder
Differentials- kidney disease, haemoglobinuria, myoglobinuria, food dye.

72
Q

Proteinuria symptoms

A

Frothy urine
Oedema due to reduced plasma oncotic pressure
Loss Ig= infection prone
Prothrombotic.

73
Q

CKI

A

Often late px- renal impairment, HTN, dipstick abnormailty, uraemia syndrome.
-symptoms-
None until eGFR under 30ml/min. Even then mild and non specific symptoms only.
Usually start dialysis at eGFR 8-10 before lose too much function.
Symptoms when advanced- tired, SOB, vomiting, aches, sleep reversal, nocturia, restless leg, itch, CP, seizure, coma.

74
Q

AQP

A

AQP 2 apical (luminal memrane) insertion driven by ADH.

AQP3+4 basolateral membrane, permeability not altered by ADH.

causes of signs (13 decks)

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