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Year 3 > Week 14 Renal > Flashcards

Week 14 Renal Flashcards

1
Q

3 ways to measure urinary protein excretion

A

24 hour urine collection

Spot sample (in morning) - protein:creatinine ratio

Albumin:creatinine ratio

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2
Q

3 most important measurements for kidney function

A

Creatinine

Urea

eGFR

Ideally, substance would be freely filtered at golmerulus, not secreted or absorbed

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3
Q
A
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4
Q

Creatinine

A

Muscle breakdown prouduct

More sensitive than urea

However affected by:

Muscle mass (higher with high muscle mass)

Plasma volume (increases when dehydrated)

Diet (increaes in high protein diet)

15% secreted by tubules

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5
Q

Urea

A

40% reabsorbed

Increased in diet high in protein or if there is GI bleed (as blood is digested to protein to urea)

Increased in dehydration (reabsorbed in proximal tubule)

Increased in tissue breakdown e.g. corticosteroids

Lowers in liver failure (as liver produces urea)

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6
Q

Glomerular filtration rate defintion

A

Volume of plasma which would be cleared of that substance per unit time

urine conc of substance x urine vol divided by plasma conc of substance

(ml/min)

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7
Q

MDRD4 formula

A

Estimatation of GFR from plasma creatinine conc (eGFR)

Based on:

Creatinine conc

Age

Sex

Race

(ml/min per 173m2)

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8
Q

Relationship between eGFR and creatinine

A

As eGFR falls, creatinine increases

However, can lose 50% kidney function before creatinine increases

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9
Q

Why can’t eGFR be used for AKI?

A

eGFR assumes stable renal function

(so not sutiable for AKI)

Important for drug dosing

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10
Q

Glomerulonephritis

A

Group of inflammatory diseases involving glomerulus and tubules

Primary: limited to kidney

Secondary: due to underlying cause e.g.

  • infections: HIV
  • inflammatory conditions: IBD, RA,
  • drugs: NSAIDs
  • malignancy: lung cancer

Symptoms: Haematuria, oliguria, oedea, HTN

Pathophysiology:

Glomerular injury caused by inflammation due to extrinsic or intrinsic factors:

Extrinsic: antibodies, complement

Intrisnic: cytokines, growth factors

Examples:

IgA Nephropathy

Membranous GN

Minimal change disease

RPGN (rapidly progressing glomerular nephritis)

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11
Q

Clinical presentations of glomerulonephritis

A

Nephritic: blood and protein in urine, high BP, rising serum creatinine

proliferative/acute inflammation

IgA/lupus nephritis

Nephrotic:

>3.5 proteinuria, low seurum albumin, oedema

Non-proliferative/podocyte damage

Minimal change disease 1, membranous

Rapidly progressing glomerulonephritis

Rapidly increasing serum creatinine, crescentic damage

Vasculitis, lupus nephritis

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12
Q

3 features of nephrotic syndrome

A

>3.5g proteinuria (per 24hrs)

Low serum albumin <30

Oedema

Also have hyperlipidaemia, risk of venous thromboembolism, hypercoagulable state (due to loss of anti-thrombin III)

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13
Q

IgA nephropathy

A

Most common primary glomerular disease

Can be precipitated by infection - synpharyngitic (occurs same time as pharyngitis)

May be secondary to ceoliac disease, cirrhosis

Pathophysiology:

Abnormal/overproduction of IgA which deposit in mesangial cells leading to mesangial proliferation

Symptoms:

Haematuria, HTN, proteinuria

1/3 progress to ESRF

Treatment: ACEi

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14
Q

Membranous GN

A

Presents with nephrotic syndrome

Most common in caucasians

Primary: idiopathic

Secondary: Malignancy (e.g. lung cancer), drugs (e.g. NSAIDs), SLE

Pathophysiology:

Immune complexes deposited into glomerular BM - thickening and damaging BM - increased permeability - proteinuria

70% pts with Anti-phopholipase A2 receptor antibody (PLA2R) (protein on podocytes)

Variable history:

1/3 resolve, 1/3 progress to ESRF, 1/3 persistent proteinuria, maintain GFR

Treatment:

Treat underlying disease if secondary

Non-immunological: ACEi, statins, diuretics, low salk diet

Immunological: Steroids, cyclophosphamide, ciclosporin, rituximab (Anti-CD20 (B cells))

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15
Q

Minimal change disease

A

Commonest form of GN in children, characterised by minimal histological changes

Causes nephrotic syndrome (proteinuria, oedema, hypoalbuminaemia, hyperlipidaemia)

First presentation: periorbital oedema

GFR normal

Primary: idiopathic

Secondary: malignancy

May occur after URTI

Pathogenesis: T cell mediated. Podocytes fuse/merge together, causes leakiness of protein into urine

Normal glomeruli on H and E stain

Assoc. with Hodgkin’s Lymphoma

Treatment: Prednisolone (as damaged mediated by cytokoines due to T cells)

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16
Q

Rapidly progressing glomerulonephritis

A

Group of conditions which show golmerular crescents on kidney biopsy

Aggressive - 90% pts progress to ESRF

Causes: ANCA vasculitis (small vessel vasculitis) e.g. granulomatous with polynagiitis, Lupus nephritis, Goodpasture’s syndrome (antibodies to glomerular BM), post-infection, Henoch Schonlein Purpura

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17
Q

Investgiations for Glomerulonephritis

A

UEs, urine dip, 24- hour urine collection (quantify protein), serum albumin, renal US

Glomerulonephritis screen:

HbA1c/plasma glucose - diabetic nephropathy

ANCA - vasculitis

PLA2R - membranous GN

ANA,complement - lupus

Kidney biopsy: required for clinical diagnosis of glomerulonephritis

  • biopsy cortex, examine:

light microscopy: structure

immunofluorescnece: Ig, complement

electron microscopy: BM, deposits

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18
Q

Systemic diseases assoc with renal disease

A

Diabetes

Atheromatous vascular disease

Amyloidosis

SLE

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19
Q

How do systemic diseases present in kidneys?

A

AKI (creatinine increases)

CKD

Proteinuria

Nephrotic syndrome (creatinine normal, proteinuria)

Nephritic syndrome (high creatinine, blood/protein in urine)

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20
Q
A
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21
Q

Risk factors for UTI

A

Less than 1 yrs old

50% children with UTI have congenital renal tract abnormality (commonly vesico-ureteric reflux)

Females - sex

Men - prostate enlargement

Diabetes

Immunosuppression

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22
Q

UTI in childhood - incidence vs age

A

Males 50% <1 yrs

Females >80% >1yrs old (more common due to short urethra)

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23
Q

UTI symptoms of upper vs lower

A

Pyelonephritis (Upper urinary tract infection)

Bacteriuria and fever >38

Bacteriuria and loin pain, fever <38

Symptoms:

Fever, general malaise, loin pain

Cystitis (lower urinary tract infection)

Bacteriuria, symptoms UTI not systemic

Symptoms: Abdo pain, urgency, frequency

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24
Q

Investigations UTI

A

Urine dip stick

Lecuocyte esterase (LE) - correlates with WBCs

Nitrites (bacteria convert nitrates into nitrites)

Microscopy/flow cytometry

Urine culture - gold standard. Required for all children <3yrs before antibiotics.

> 10^5 CFU (colony forming units)

Most common organisms: E.coli, Klebsiella, proteus (stone former), streptococcus (gram +ve)

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25
Q

UTI management for children

A

Test urine when infant or child presents with unexplained fever, symptoms/signs suggestive UTI

Oral antibiotcs unless severely ill, vomiting, infants<3 months

Oral: trimethoprim, nitrofurantoin

IV antibiotics:

IV Ceftriaxone

IV Gentamicin

Antibiotic prophylaxis:

Consider for CAKUT (congenital abnormalties of kidney and urinary tract)

  • Prophylaxis reduces risk of febrile UTI in vesico-ureteric reflux
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26
Q

UTI in children definition

A

Bacterial infection of lower uriSavenary tract (cystitis) or upper urinary tract (pyelonephritis), or both.

Cystitis (type of UTI due to infection of lower urinary tract)

Bacteriruria with symptoms of UTi, not systemic:

Symptoms: Dysuria, frequnecy, urgency

Pyelonephritis (type of UTI due to infection upper urinary tract (due to ascending bacteria))

Bacteriruia with fever >38

Symptoms: systemic - fever, malaise, flank pain + symptoms of cystitis

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27
Q

3 complications of UTI in children

A

Renal scarring

HTN

CKD

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28
Q

3 risk factors renal scarring

A

Vesico-ureterical reflux

Anatomical obstruction

Dysfunctional voiding

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29
Q

CAKUT

A

Congenital abnormalities of kidneys and urinary tract

Vesico-ureterical reflux (valve defect)

Obstruction of urinary drainage tracts

Both assoc. with congenital renal dysplasia

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30
Q

Adukt Polcystic Kidney Disease

A

Disorder characterised by renal cysts and systemic manifestations.

Commonest inherited disorder in kidneys

AD

Causes:

Mutations in PK1 (85%) and PK2 (15%) which are encode polycystin 1 and 2 (present in renal tubule epithelium (and liver/pancreas)

  • Leading to overexpression in cyst cells - cyst formation.

PK1 more severe

25% pts no family history

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31
Q

APKD clinical presentation and diagnosis

A

Presents with family history

Symptoms: HTN, abdo pain, renal cysts

Signs: Palpable renal mass

Diagnosis:

If have family history, US when they are 21yrs, if negative, US at 30 yrs

<30 yrs: 2 cysts

30-59: 2 cysts each kidney

>60: 4 cysts each kidney

If no family history: >10 cysts in both kidneys

CT/MRI pelvis/abdomen

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32
Q

APKD complications

A

Renal: End stage renal disease, cyst problems e.g. bleeding, pain, replaces normal tissue

Other: HTN, intracranial aneurysms, liver/pancreatic cysts

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33
Q

Management APKD

A

Supportive

Manage HTN

Tolvaptan (Vasopressin V2 receptor antagonist) - decreaes cyst formation, delays decline in renal function

SE: hypernatraemia (increased Na+) and hepatotoxicity

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34
Q
A
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35
Q

Alport’s syndrome

A

X-linked

Mutations in COL4A3, 4, 5, which encodes alpha 3, 4, 5 chains of collagen 4 (main component in GBM). Leads to lamination and splitting of GBM.

Clinical consequences:

Microscopic haematuria, proteinuria, ESRF

Sensorineural deafness (childhood)

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36
Q

Other cystic kidney diseases

A

AR PKD - children

Von Hippel Lindau (AD) - malignant, benign tumours

Tuberosclerosis (AD) - benign brain tumours, learning difficulties

Medullary cystic disease (AD) - cysts in medulla, gout

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37
Q

Fabry’s disease

A

X-linked storage disease

Mutation leading to decreased enzyme, alpha galactosidase A which causes increased Gb3 (globotriaosylceramide) in podocytes

Causes proteinuria, ESRF

Symtpoms: cutanoues lesions - angiokeratoma

Diagnosis: alpha-Gal A in leukocytes

Renal biospy: inclusion bodies of Gb3

Treatment: enzyme replacement

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38
Q

Diabetic nephropathy (definition, pathophysiology, structural changes, treatment)

A

Macroalbuminuria or microalbuminuria, assoc. with retinopathy (TMD1/2)

Pathophysiology:

Hyerpglycaemia - increased pressure in glomerulus - hyperfiltration - proteinuria - HTN and renal failure (20 years)

Structural changes: BM thickening, loss of podocytes, mesangial expansion

Histology: Wilson nodule (areas of mesangial expansion)

Treatment: Glycaemic control, ACEi, SGLT2 inhibitors (as causes glucose excretion, and natriuresis (due to Na+ reabsorption with glucose, leading to activation RAAS)

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39
Q

Atheromatous vascular disease (Renal artery stenosis)

A

DD: Obstruction, interstitial nephritis

Renal artery stenosis: narrowing of renal artery. Clinical diagnosis.

Pathophysiology:

Atheroma - progressive narrowing - decreased GFR - hypoxia in renal cortex - microvascular damage - parenchyma inflammation - fibrosis

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40
Q

AKI

A

Decline in renal excretory function over hours/days and increased in serum creatinine and urea

Assessment:

KDIGO

Stage 1: serum creatinine >1.5, <2

Stage 2: serum creatinine >2, <3

Stage 3: serum creatinine > 3

x increase AKI baseline

Management:

Airway

Breathing

Circulation - restore renal perfusion

  • correct hyperkalaemia, pulmonary oedema

Remove causes e.g. drugs, sepsis

Exclude obstruction

Hyperkalaemia treatment:

6-6.4: risk of arrythmia

>6.5 is medical emergency

Causes ECG changes: ventricular tacycardia - loss of P wave, peaked T wave

  • IV calcium gluconate
  • Insulin/dextrose (drives K+ into cells)

Oral calcium resonium (reduce absorption)

Bicarbonate (if high K+, and HCO3 <16)

Dialysis (if refractory hyperkalaemia, pulmonary oedema, acidotic, toxins)

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41
Q

3 types of AKI

A

Pre-renal (decresaed perfusion)

  • Hypotension
  • Sepsis (cause vasodilation causing drop in perfusion pressure)
  • Cardiac failure
  • ACEi
  • Renal artery stenosis

Renal

Acute tubular necrosis (most common)

Obstructive

GN

Vasculitis

Gentamicin

Rhabdomyolysis

Post-renal (obstruction)

  • Calculi
  • Tumours e.g. prostate
  • Lymph nodes
42
Q

ATN (acute tubular necrosis)

A

Most reversible

Necrosis of tubular cells causing obstruction of tubules

Symptoms: hypotension, tachycardia

Causes:

Ischaemia - hypotension, sepsis

Toxins:

Endogenous - myoglobin (due to rhabdomyolysis. Presents with coca-cola urine), Ca2+

Exogenous - NSAIDs, gentamicin, ACEi, radiocontrast

Complications: polyuric phase (up to 72 hrs), inability to concentrate urine in tubules

43
Q

CKD: definition, causes, signs/symptoms, investigations

A

Kidney damage or eGFR <60ml/min for 3 months or more

Causes:

Diabetic nephropathy, chronic glomerulonephritis, APKD, reflux nephropathy

Symptoms: Itch, rotten taste in mouth (due to uraemia), fatigue (due to anaemia), weight loss, SOB, joint/bone pain

Signs: Pulmonary oedema, HTN, increased HR, yellow tinge skin (uraemic frost)

Investigations:

FBC: Anaemia

Ca2+ (decreased), PTH (incresead), phosphate (increased)

  • Kidney’s can’t excrete phosphate, and 1a hydroxylate Vit D causing decreased Ca2+. PTH increaesd to compensate (resorbs bone, also increases phosphate)

Serum creatinine (increased)

Urinalysis (proteinuria, haematuria)

eGFR (decreased)

Renal US (kidneys smaller than normal if chronic, and to see if there is obstruction)

Staging:

Stage 1: >90

Stage 2: 60-89

Stage 3: 30-59

Stage 4: 15-29

Stage 5: <15

Stage 1 and 2 normal, unless urine or structural abnormality e.g. proteinuria, APKD

44
Q

What happens to afferent and efferent arterioles as GFR falls?

A

Prostaglandins dilate afferent arterioles (to increase flow)

Ang II constricts efferent arteriole

NSAIDs inhibit prostaglandins, ACEi inhibits Ang II, so contra-indicated for AKI

45
Q

Things to slow progression of AKI

A

BP control

Glycaemic control

Diet

Smoking

Lowering cholesterol

Treat acidosis

46
Q

Treatment CKD

A

1st line treatment ACEi e.g. Ramipril

  • Can be used as 25% GFR reduction in first few weeks is a good thing

2nd line: Ca+ channel blockers e.g. verapimil

Activated Vit D (Alfacalcidol)

Phosphate binders e.g. calcium carbonate

Cinalcalcet (calcimimetic) - to decrease production of PTH

47
Q

4 functions of kidney

A

Regulates total body water

Regulates electrolytes

Makes EPO

Makes renin

48
Q

Indication renal replacement therapy

A

Medically resistant HTN

Medically resistant pulmonary oedema

Medically resistant acidosis

Uraemic pericarditis

Uraemic encephalopathy

No rule for eGFR, but usually 5-10

49
Q

4 types of renal replacment therapy

A

Haemodialysis

Peritoneal dialysis

Renal transplant

Conservative treatment

50
Q

Haemodialysis

A

Removal of solutes through diffusion

Removal of fluid through pressure: hydrostatic filtration

Uses external semi-permeable membrane

Requires AVF (arterial venous fistula) - artery and vein connected

Pros:

Hospital or home

4h, 3 times a wk

Home based more flexibile, but requires carer, space

Cons:

Acute hypotension “crash”

Access problems

Cramps

51
Q

Peritoneal dialysis

A

Diffusion and osmotic filtration

Across peritoneal membrane as filter

Dialysis fluid goes in via catheter (contains high amounts of glucose - hyperosmolality) causing osmotic filtration

Types:

CAPD (continuous ambulatory peritoneal dialysis)

  • occurs during day

APD (automated peritoneal dialysis)

  • occurs during night

Pros:

Home based

Maintain independence

Cons:

Infection - peritonitis

Glucose load - develop/worsen diabetes

Obese pts, intra-abdominal adhesions not suitiable

52
Q

Problems not helped by dialysis

A

EPO, iron supplements needed

Renal bone disease - need phosphate binders, vit D

Neuropathy

53
Q

When to treat asymptomatic bacteruria

A

Preschool children

Pregnancy

Immuncompromised

Renal transplant

54
Q

UTIs causes

A

90% caused by single organism

E.coli, Klebsiella, Proteus, Enterococcus

Multiple in:

Catheters, recurrent infection

Multi-drug resistant bacteria:

Frequent infections, mutiple antibiotic courses

55
Q

Renal transplant

A

Types:

Living or cadaveric (after brainstem, cardiac death)

Average wait 3 years

Pros:

No dialysis

More independence

Better renal function

Cons:

Requires immunosuppressants after e.g. ciclosporin, tacrolimus

Increased cardiovascular risk

Increased infection

Contraindications:

Malignancy

Active infection

56
Q

Clinical features in adult UTI

A

Suprapubic discomfort, dysuria, frequency, urgency, low grade fever

Nocturia, incontinece in elderly

57
Q

Investigations uncomplicated UTI

A

If first time presenation in non-pregnant women: urine dipstick, culture not mandatory

Children and men require urine culture always

58
Q

Treatment UTI pregnancy

A

Amoxillcin or Cefalexin

59
Q

Treatment recurrent UTI

A

2 or more episodes in 6 months

3 or more in 1 years

Management:

Oral hydration

Post-coital voiding

oral estrogen

Short course antibiotics

Single post coital antibiotics

Prophylactic abx - if other measure failed

60
Q

Complicated UTIs

A

IV Ciprofloxacin

Catheter assoc. UTI

Organisms usually pts flora or healthcare environment

Complications CAUTI:

  • chronic renal inflammation
  • Risk of bladder Ca

Treatment: IV Gent

Renal pyelonephritis

Upper UTI infection, ascending infection involving pelvis of kidney

Complication: renal abscess (usually gram -ve)

  • Can lead to emphysematous pyelonephritis (severe infection that causes gas accumulation in tissue)

Perinephric abscess

Pus in perinephric space

Pts usually septic

Causes:

Untreated lower UTI, anatomical abnormalities

Organisms: E.coli, S. aureus

Management:

FBC, UEs, CRP, urine sample, blood culture, renal US, abx

61
Q

Acute bacterial prostatitis

A

Inflammation of prostate due to bacterial infection

Symptoms: Fever, back pain, acute lower UTI symptoms e.g. dysuria, frequency, uregency

Organisms: E.coli, S.aureus, N.gonnorhoea

Complications: Prostate abscess, rupture

Treatment: IV Ciprofloxacin

62
Q

Chronic prostatitis

A

Prolonged prostate infection lasting >3 months

Asymptomatic, fever, back pain, UTI symptoms

Organisms: E.coli, Enterococcus, S.aureus

63
Q

Orchitis and Epididymitis

A

Orchitis

Inflammation of one/both testicles

Symptoms: testicular pain, fever, dysuria

Causes: bacterial or viral e.g. mumps

Bacterial orchitis: complication of epididymitis

Epididymitis

Inflammation of epididymis

Ascending infection from urethra

Causes: Gram neg, TB

64
Q

Fournier’s Gangrene

A

Type of nec fas affecting genital, perineum

Rapid onset, systemic sepsis

Organisms: E.coli, anaerobes

Risk factors: UTI, IBD complications

Treatment: surgical debridement

65
Q

Urine microscopy interpretation (Epithelial cells, bacteria no WBC, bacteria + WBCs +/- cathether, Pyuria with no bacteria)

A

Epithelial cells: contamination

Bacteria no WBC: contamination

Bacteria + WBCs, with catheter: assess clinically

Bacteria + WBCs + no catheter: infection

Pyuria (pus in urine) with no bacteria: TB, urethritis (chlamydia), previous antibiotcs

66
Q

Nephrolithiasis

A

Colicky pain, haematuria, unilateral flank tenderness

Calcium oxalate/phosphate (most common)

Cause: Idiopathic, hypercalciuria

Infection stones:

struvite (Magneusium, ammonium, phospate) - proteus

Uric acid stone (not seen on XR) - most common seen in gout, hyperuricaemia

Others: cystiene (not seen on CT) - mostly in children

67
Q

Volume of distribution definition

A

Volume in which the amount of drug needed to distribute uniformly to produce observed blood conc (tells you how extensively the drug distributes to rest of body compared to plasma)

Vd increased in lipid soluble drugs e.g. diazepam

If Vd near the plasma drug conc, shows drug stays in vascular space e.g. warfarin

68
Q

PK vs PD

A

PK: what body does to drug

  • Absorption
  • Distribution
  • Metabolism
  • Excretion

PD: what drug does to body

  • MOA of drug
  • Efficacy
  • Safety profile
69
Q

Clearence

A

Volume of plasma needed to clear substance per unit time

70
Q

Half life

A

Time required for serum plasma conc of the drug to decrease by half

Long half life required loading dose

4-5 half lives to reach steady state

Depends on clearence and Vd

Used to determine:

Time it takes for drug to be eliminated

Time to reach steady state

Dosing interval

71
Q

Linear vs non-linear pharmacokinetics

A

Linear: dose proportional to conc of drug e.g. double dose, double conc

Rate of elimiation proportional to conc

Non linear: dose non-proportional to conc

Rate of elimiation constant regardless of drug conc.

72
Q

What factors influence PK/PD

A

Age

Renal impairment

Hepatic impairement

Congestive HF

GI disease

73
Q

How does age influence PK?

A

Decreased total body water and increased fat - affects Vd

Water soluble drugs e.g. lithium, gentamicin

  • Serum levels may increaese due to decreased Vd

Fat soluble drugs e.g. diazepam

  • Half life may increase with increaesd body fat

B-blockers effect reduced in age

74
Q

Cockroft and Gault equation

A

Creatinine clearence

Depends on age, weight, sex, creatinine conc

75
Q

Exmaples of drug- disease interactions

A

PD pts have increased risk of drug induced confusion

NSAIDs can exacerbate CHF

76
Q

Examples of drug drug interactions in eldery

A

Statins and erythromycin

Verapamil and B-blockers

77
Q

Common examples of pescribing cascade in elderly

A

NSAIDs - HTN - antihypertensives

Ca channel anatagonists - oedema - furosemide

78
Q

What drugs causes decreased elimiation in renal disease?

A

Gentamicin

Lithium

Digoxin

Methotrexate

Penicillins

79
Q

Renal failure and acidic drugs

A

Renal failure can lead to acidosis

Acidic drugs less bound to albumin (ionised) leading to more free (active) drug in plasma

E.g. phenytoin (acidic)

80
Q

What do with antibiotics and LMWH, pheytoin, digoxin in renal disease?

A

Reduce dose

81
Q

What to do with metformin, NSAIDs?

A

Avoid

82
Q

What to do in ACEi in renal disease?

A

Caution

83
Q

Renal disease vs heptic disease PD/PK

A

Renal:

Same/Increased Vd, decreased rate of excretion (t1/2 increased)

Increase dosing interval

Hepatic:

Same/incresed Vd, slower rate of metaoblism (t1/2 and F increases)

Reduce dose, increase dosing interval

84
Q

Liver disease high vs low extraction drugs

A

High extraction: metabolised at high rate by liver. Affected by changes in blood flow. E.g. Morphine

Low extraction: metabolised at low rate by liver. Not changed by blood flow. But changes with liver enzyme activity. E.g. theophylline

85
Q

Effect on pharmacodynamics on liver disease

A

Increased sensitvity to oral anticoagulants

Fluid retention

Hepatorenal syndrome

86
Q

Causes of renal stone foramtion?

A

Abnormal urine (e.g. too much salt)

Urinary obstruction e.g. pelviureteric junction obstriction, medullary sponge kidney

UTI (proteus mirablis splits urea into ammonia, causing alkaline pH leading to struvite stones)

87
Q

What causes abnormal urine?

A

Too much salt

  • Salt can lead to increaesd acid (metabolic syndrome), hypercalciuria

Not enough water

Lack of inhibitors e.g citrate, magnesium

88
Q

Type of stones

A

Calcium oxalate or phosphate (most common)

Struvite

Uric acid

Others e.g. Cysteine

89
Q

Management of stones

A

Observation

Medical: NSAIDs (reduces pain, GFR and renal pressure)

Surgical:

ESWL (extracorporeal shockwave lithotripsy)

  • shockwaves to break up stones
  • proximal utreteric stones <10mm, or renal stones <2cm

Laproscopy/open surgery

  • treat huge
    ureteric stones, non functioning kidney
90
Q

Sepsis and osbtructing stone

A

Medical emergency

Implement sepsis 6

Invstigations:

Bloods, CRP, Coag

USS or CT

Treatment: Nephrostomy (tube placed into kidney to drain urine out) or ureteric stent

91
Q

Fluids

A

Maintenance:

0.18% NaCl

5% glucose

Hartmann’s

Replacement:

Hartmann’s

Alternative balanced solutions for resus

Resusication:

Hartmann’s

Alternative balanced solutions for resus

92
Q

Problems with 0.9% saline

A

Not physiological

Can cause hyperchloraemia acidosis

Increaesd Cl+ leads to renal vasoconstriction leading to poor UO

Kidney’s can’t excrete Na+ load

So leads to hyperchloraemia, hypernatraemia, acidosis

93
Q

Rhabdomyolysis

A

Damaged skeletal muscle breaks down, releasing myoglobin, intracellular ions

Due to trauma, prolonged immobilisation (e.g. due to alcohol, drugs)

Leads to:

  • electrolyte imbalance (high K+, Mg, phosphate, low Ca+)
  • DIC (increased PT, PTT and INR)
  • AKI (increaed urea, creatinine)

Diagnosis: Increased serum creatinine kinase 5x ULN

94
Q

Differentiating between AKI and chronic kidney disease

A

Acute:

US: Normal sized kidneys

Electryolyte imbalance e.g. high K+

Chronic:

US – small kidneys

PTH elevated

Phosphate elevated

Anaemic

95
Q

Causes of bladder obstruction

A

Posterior urethral valve

- Obstructing membrane at posterior urethra due to abnormal development

  • Most common congenital cause of bladder obstruction
  • Presents as antenatal hydronephrosis, UTI

Management: valve resection

Prostate hypertrophy

Neurogenic bladder e.g. spinal bifida

PUJO (pelvi-ureteric junction obstruction)

Between renal pelvis and ureter

Common cause of hydronephrosis in children

Commonly found on antenatal US

Abdo mass, haematuria

VUJO (vesico ureteric junction obstruction)

Between ureter and bladder

Anantomical narrowing or obstruction e.g. strictures

Abdo mass, haematuria

96
Q

Prostate Ca

A

Adenocarcinoma, usually arises in periphary of prostate

Risk factors: Age, genetics e.g. BRAC2, p53, african american

Signs/symptoms:

Often asymptomatic, UTI, haematuria, bone pain (most common symptom of metastases)

Complications:

SC compression, ureteric obstruction

Diagnosis:

Digital rectal exam

PSA (prostate specific antigen)

TRUS (needle biopsy)

Gleeson Grading (based on how differentiated they are) - provides prognostic information

TNM staging

Treatment

Radiotherapy

Androgen ablation - LHRH analogue, or orchidectomy (surgical castration)

Chemotherapy

Prostatectomy

97
Q

Bladder Ca

A

Transitional cell carcinoma

Risk factors: Age, caucasian, chronic inflammtion e.g. stones, long term catheters

Presents: Painless, visible haematuria

Diagnosis: Cystoscopy

Treatment:

TURBT (trans-urethral resection, of bladder tumour)

Cystectomy (bladder and prostate/uterus removed)

Mets: usually pulmonary

M-VAC (Methotrexate, vinblastine, doxorubicin, cisplatin)

98
Q

Renal carcinoma (risks, investigations, histology, treatment)

A

Renal cell carcinoma (most common)

Risk factors:

Smoking, obesity, HTN, renal cysts, haemodialysis

Presents: triad: mass, pain, haematuria

lower leg oedema, paraneoplastic syndrome: polycytheamia (increased EPO), HTN, (increased renin),

Investigations:

FBC, CRP, LFTs, bone profile, US, CT kidneys, renal biopsy

Histology:

Clear cell (most common) - vascular, granular and clear (due to lipids)

Papillary - sold, multi-focal

Treatment:

Nephron sparing surgery (part of kidney removed) - if pt ahs one kidney, CKD

Radical nephrectomy (remove kidney)

Mets: Tyrosine kinase inhibitors

99
Q

Testicular and penile cancer

A

Germ cell tumours (most common), Stromal tumours

Most curable ca.

Risk factors: Age: 25-40, cryptochordism, HIV

Presentation: painless lump,

Investigation:

Alpha-feta protein (also in HCC)

Beta hCG

LDH

Treatment:

Radical orchidectomy, chemo

Penile cancer:

Risk factors: HPV 16, 18, smoking

Treatment:

Circumcision, penectomy+/-reconstruction

100
Q

UTI in children investigations

A

Renal US

Pros: Dilated ducts, no radiation

Cons: Can’t see kindey parenchyma

Micturating cystourethrogram

Dye given through cathether, X rays taken. Shows flow of urine

Pros: GS for VUJ

Cons: radiation

Nuclear:

DMSA

Radiocontrast given, taken up by healthy tissues

Pros: Scarring

Cons: GS Radiation

MAG3 indirect cystogram

Radiocontrast injected, passed out into urine

Pros: VUJ, no catheter required

Cons: Continence and co-operation required

MAG3 diuresis renogram

Pros: GS for obstruction

Cons: continence and co-operation

Year 3 (15 decks)

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