Week 14 Renal Flashcards

(100 cards)

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
UTI management for children
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
26
UTI in children definition
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
27
3 complications of UTI in children
Renal scarring HTN CKD
28
3 risk factors renal scarring
Vesico-ureterical reflux Anatomical obstruction Dysfunctional voiding
29
CAKUT
Congenital abnormalities of kidneys and urinary tract Vesico-ureterical reflux (valve defect) Obstruction of urinary drainage tracts Both assoc. with congenital renal dysplasia
30
Adukt Polcystic Kidney Disease
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
31
APKD clinical presentation and diagnosis
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
32
APKD complications
Renal: End stage renal disease, cyst problems e.g. bleeding, pain, replaces normal tissue Other: HTN, intracranial aneurysms, liver/pancreatic cysts
33
Management APKD
Supportive Manage HTN Tolvaptan (Vasopressin V2 receptor antagonist) - decreaes cyst formation, delays decline in renal function SE: hypernatraemia (increased Na+) and hepatotoxicity
34
35
Alport's syndrome
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)
36
Other cystic kidney diseases
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
37
Fabry's disease
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
38
Diabetic nephropathy (definition, pathophysiology, structural changes, treatment)
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)
39
Atheromatous vascular disease (Renal artery stenosis)
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
40
AKI
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)
41
3 types of AKI
**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
ATN (acute tubular necrosis)
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
CKD: definition, causes, signs/symptoms, investigations
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
What happens to afferent and efferent arterioles as GFR falls?
**P**rostaglandins **d**ilate **a**fferent arterioles (to increase flow) **A**ng II constricts **e**fferent **a**rteriole NSAIDs inhibit prostaglandins, ACEi inhibits Ang II, so contra-indicated for AKI
45
Things to slow progression of AKI
BP control Glycaemic control Diet Smoking Lowering cholesterol Treat acidosis
46
Treatment CKD
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
4 functions of kidney
Regulates total body water Regulates electrolytes Makes EPO Makes renin
48
Indication renal replacement therapy
Medically resistant HTN Medically resistant pulmonary oedema Medically resistant acidosis Uraemic pericarditis Uraemic encephalopathy No rule for eGFR, but usually 5-10
49
4 types of renal replacment therapy
Haemodialysis Peritoneal dialysis Renal transplant Conservative treatment
50
Haemodialysis
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
Peritoneal dialysis
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
Problems not helped by dialysis
EPO, iron supplements needed Renal bone disease - need phosphate binders, vit D Neuropathy
53
When to treat asymptomatic bacteruria
Preschool children Pregnancy Immuncompromised Renal transplant
54
UTIs causes
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
Renal transplant
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
Clinical features in adult UTI
Suprapubic discomfort, dysuria, frequency, urgency, low grade fever Nocturia, incontinece in elderly
57
Investigations uncomplicated UTI
If first time presenation in non-pregnant women: urine dipstick, culture not mandatory Children and men require urine culture always
58
Treatment UTI pregnancy
Amoxillcin or Cefalexin
59
Treatment recurrent UTI
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
Complicated UTIs
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
Acute bacterial prostatitis
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
Chronic prostatitis
Prolonged prostate infection lasting \>3 months Asymptomatic, fever, back pain, UTI symptoms Organisms: E.coli, Enterococcus, S.aureus
63
Orchitis and Epididymitis
**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
Fournier's Gangrene
Type of nec fas affecting genital, perineum Rapid onset, systemic sepsis Organisms: E.coli, anaerobes Risk factors: UTI, IBD complications Treatment: surgical debridement
65
Urine microscopy interpretation (Epithelial cells, bacteria no WBC, bacteria + WBCs +/- cathether, Pyuria with no bacteria)
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
Nephrolithiasis
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
Volume of distribution definition
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
PK vs PD
PK: what body does to drug - Absorption - Distribution - Metabolism - Excretion PD: what drug does to body - MOA of drug - Efficacy - Safety profile
69
Clearence
Volume of plasma needed to clear substance per unit time
70
Half life
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
Linear vs non-linear pharmacokinetics
**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
What factors influence PK/PD
Age Renal impairment Hepatic impairement Congestive HF GI disease
73
How does age influence PK?
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
Cockroft and Gault equation
Creatinine clearence Depends on age, weight, sex, creatinine conc
75
Exmaples of drug- disease interactions
PD pts have increased risk of drug induced confusion NSAIDs can exacerbate CHF
76
Examples of drug drug interactions in eldery
Statins and erythromycin Verapamil and B-blockers
77
Common examples of pescribing cascade in elderly
NSAIDs - HTN - antihypertensives Ca channel anatagonists - oedema - furosemide
78
What drugs causes decreased elimiation in renal disease?
Gentamicin Lithium Digoxin Methotrexate Penicillins
79
Renal failure and acidic drugs
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
What do with antibiotics and LMWH, pheytoin, digoxin in renal disease?
Reduce dose
81
What to do with metformin, NSAIDs?
Avoid
82
What to do in ACEi in renal disease?
Caution
83
Renal disease vs heptic disease PD/PK
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
Liver disease high vs low extraction drugs
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
Effect on pharmacodynamics on liver disease
Increased sensitvity to oral anticoagulants Fluid retention Hepatorenal syndrome
86
Causes of renal stone foramtion?
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
What causes abnormal urine?
Too much salt - Salt can lead to increaesd acid (metabolic syndrome), hypercalciuria Not enough water Lack of inhibitors e.g citrate, magnesium
88
Type of stones
Calcium oxalate or phosphate (most common) Struvite Uric acid Others e.g. Cysteine
89
Management of stones
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
Sepsis and osbtructing stone
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
Fluids
**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
Problems with 0.9% saline
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
Rhabdomyolysis
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
Differentiating between AKI and chronic kidney disease
Acute: US: Normal sized kidneys Electryolyte imbalance e.g. high K+ Chronic: US – small kidneys PTH elevated Phosphate elevated Anaemic
95
Causes of bladder obstruction
**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
Prostate Ca
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
Bladder Ca
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
Renal carcinoma (risks, investigations, histology, treatment)
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
Testicular and penile cancer
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
UTI in children investigations
**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