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Final > Renal > Flashcards

Renal Flashcards

1
Q

What is eGFR

A

Creatinine clearance used to estimate GFR

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2
Q

What is creatinine

A

Chemical waste product from muscle metabolism

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3
Q

Why are diuretics nephrotoxic?

A

Due to the hypovolaemia caused

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4
Q

RAAS physiology

A

RAAS activated when low BP at afferent arteriole

Secretion of renin from kidneys (juxtaglomerular cells), Renin (enzyme) converts angiotensinogen -> angiotensin, ACE in lungs converts to angiotensin II

Angiotensin II = vasoconstrictor & Stimulates aldosterone release (adrenal cortex)

Aldosterone = inc sodium and water retention, inc K+ loss

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5
Q

What is secreted during high volume? Where from?

A

ANP/BNP

From heart

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6
Q

What is Activated during low volume?

A

RAAS

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7
Q

Angiotensin II effect on kidneys

A

Constrict efferent arteriole

- This is to maintain GFR during hypotension

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8
Q

ACEi SE

A

May impair renal function (Angiotensin II efferent constriction lost) and dec GFR

Hyperkalaemia due (less aldosterone)

Bradykinin mediated cough

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9
Q

ARB (e.g. Losartan)

  • Use
  • indication
  • SE
  • CI
A

Modulation of RAAS but no dry cough (direct renin inhibitor)

HTN, HF, diabetic nephropathy

Renal impari, hyperkalemia

Preg, use with other RAAS drugs

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10
Q

Where is Na+ reabsorbed

A

70% proximal tubule

25% loop of Henle

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11
Q

Potassium control kidney

A

Free filtration in proximal tubule/loop of henle

Distal secretion determines secretion (collecting duct - Aldosterone mediated)

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12
Q

Meds causing hypokalaemia

A

Loop diuretics
Thiazide diuretics

Na+ retaining diuretics

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13
Q

Meds causing Hyprekalaemia

A

(drugs causing aldosterone block or reduction)
Spironolactone
Amiloride
ACEi, ARB

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14
Q

Important roles of Kidneys:

A
  • Fluid and electrolyte balance
  • BP control
  • Activates Vti D: Ca absorption, PO4 secretion
  • EPO production: at low GFR anaemia can occur
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15
Q

What makes up glomerulus

A

Capillary bed + Bowman’s capsule

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16
Q 
Osmolarity
PCT
DescendingLH
DCT
CD
A

300mOsm

600->1200mOsm (At bottom)

100-300 mOsm

1200mOsm

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17
Q

Where is the majority of water reabsorbed

A

Descending loop of Henle

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18
Q

Site where they work:

  • Carbonic anhydrase inhibitors
  • Furosemide (loop diuretic)
  • Thiazides (indapemide)
  • K+ sparing (Spironolactone)
  • Desmopressin
A

Carbonic anhydrase inhibitors
- Proximal convoluted tubule

Furosemide
- Thick ascending loop of Henle

Thiazides
- Distal convoluted tubule

K+ sparing
- Cortical Collecting duct

Desmopressin
- ADH agonists (Vasopressin receptors in Kidney)

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19
Q

Proximal convolute tubule:

- What is reabsorbed here

A

70% filtrate
Most essential things
- 100% glucose and Aminos (passive and active transport)
- Ions: Na (Na2HCA3 or NaCl), K+, Cl

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20
Q

Loop of Henle

  • Main job
  • Key luminary’s transporter (on urine side)
  • Diuretic with action here
  • effect of diuretic and why
A

Descending limb reabsorbs water

Ascending limb concentrates or dilutes fluid in urine

20% of Na reabsorption

NKCC2 (Na, K and 2X Cl)

Inhibit NKCC2 - hypotension, hyponatraemia, hypokalaemia, hypochloraemia, indirect hypomagnesia/ hypocalcaemia/alkalosis

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21
Q

Distal convoluted tubule and Collecting duct:

  • Na reabsorption
  • Transporters
  • Hormone action here
A

5% at early DCT

Sodium/Potassium ATPase

Sodium reabsorption regulated by aldosterone (stim) and ADH (inhibit)

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22
Q

DCT

  • function
  • channel
  • Horomones (and effect)
  • diuretic:
A

Reabsorbs Na and swaps for either H+ or K+ (they compete) via aldosterone
Acidifies urine

Na/Cl passive cotransporter (reabsorbes Na and H2O)
Na/K

PTH + Vit D: Ca absorbed, PO4 secreted

Aldosterone: Na absorption
ANP: Na excretion

Thiazide (e.g. indapemide): Hypotension, hyponatraemia

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23
Q

Collecting duct:

  • function
  • Channels
  • Hormones
A

Concentrates urine

Apical (urine side)
ENaC (reabsorption of sodium) and ROMK (potassium secretion)

Basolateral (blood side of cell)
Na/K - at BV

Aldosterone, ADH (Vasopressin)

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24
Q

Renal tubular acidosis:

  • What is happening
  • What is the result
A

Dec H+ excretion or Dec reabsorption of Bicarbonate

Metabolic acidosis with normal anion gap (Even if low bicarb, renal tubule acidosis is hyperchloraemic)

Affects children

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25
Q

Causes of Renal tubular acidosis

A

Type 1) Mutation of proton pump (H-ATPase) giving inability to excrete H+ in distal tubule

Type 2) Sodium bicarb co-transporter mutation = inability to reabsorb bicarbonate

Fanconi’s syndrome: Myeloma proteins and various drugs cause proximal tubule injury giving inability to secrete H+

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26
Q

Renal tubular acidosis:

  • Investigations
  • Tx
A

Low serum bicarb
high chloride
Variable K+
low pH w normal anion gap

Sodium alkali or potassium alkali

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27
Q

Renal tubular acidosis Complications

A

Volume depletion: loss of Na+

Osteoporosis due to acidosis causing bone buffering (demineralisation)

Growth retardation: Acidosis = muscle catabolism

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28
Q

Causes of End-stage renal failure

A 
Glomerulonephritis
Pyelonephritis
Diabetes
PKD
End stage CKD
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29
Q

Pyelonephritis

  • Def
  • Causes
  • Route of infection
  • Epidemiology
A

Infection/inflammation of renal parenchyma, calyces and pelvis

Enteric bacteria (Escherichia coli, UPEC (Uropathic E.coli)

Ascending from Lower urianry tract or haematogenous

Women under 35 most common

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30
Q

Whe is pyelonephritis complicated

A

All men, pregnant, those with structural abnormalities (PKD, Horseshoe kidney, vesicle-ureteric reflux), immunosuppressed, (steroids, HIV, Radio/Chemo/Malig, transplant, sickle cell) Obstruction (posterior ureteral valve, stone, BPH)

More severe infection assoc with these

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31
Q

Pyelonephritis:

Pres triad

A

1) Loin pain
2) Fever, Rigors
3) Costovertebral tenderness

May also have N&V,

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32
Q

Pyelonephritis Invesitgation

A

Urine dip (Blood, protein nitrites)

Urinalysis (microscopy) - WBC/RBC

Gram stain (G-ve rods (e.coli, klebsiella)

FBC: Leukocytosis

ESR/CRP: raised

Bacteraemia (Risk Sepsis)

Imaging: Renal USS, CT, DMSA(reals structural scan)

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33
Q

Pyelonephritis Treatment & complications

A

Mild/Moderate: Ciprofloxacin

Severe/complicated:

  • Admit
  • IV ceftriaxone or ciprofloxacin
  • IV fluids
  • IV para

Complications: Renal failure, abscess formation, parenchymal scarring, recurrence

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34
Q

Renal cell carcinoma

  • Def
  • Types
  • Pres
  • What is difficulty with Tx
A

Malignancy of renal parenchyma

80% clear cell
15% papillary tumour

Often asymp
Triad:
1) Abdo mass + 
2) Haematuria + 
3) Loin/Flank pain
Also: weight loss, anorexia, malaise

High levels P-glycoprotein (multiple chemo resistant)

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35
Q

RCC

  • RF
  • What LNs 1st to be affected
  • Problem with surgery and mets
A

Smoking, obesity, HTN, age, Renal transplant, Polycystic kidney, Von Hipple Lindau

Para-aortic and Hilar LN

Very vascular - lots of bleeding

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36
Q

What is assoc with left sided RCC

A

Left sided varicocele due to invasion of Left renal vein

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37
Q

RCC Spread

Mets description

A

Direct - renal vein
LN - Paraaortic then mediastinal
Haem - Bone, Liver, Lung

Cannonball mets

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38
Q

Principles in investigating RCC

A

Check kidney function

Check structure

Check for Mets

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39
Q

RCC Ix

A

BP: inc renin = inc BP

FBC: polycythemia (EPO)

Urinalysis haematuria ± proteinuria

Cr raised with reduced clearance

Percutaneous biopsy (histology)

LFT - AST/ALT raised in mets

Abdo pelvis USS & CT - mass staging and mets (LN, Bone, Liver)

MRI for local invasion

CXR: cannonball mets to lung

Bone scan

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40
Q

RCC paraneoplastic syndrome

A 
Anaemia
Hypercalcaemia
Erythrocytosis
SIADH
Hepatosplenomegaly
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41
Q

RCC Tx & Prognosis

A

Surgical resection or Radiofrequency ablation

T3 = radical nephrectomy

T4 = Tyrosine kinase inhibitor (Sunitinib) ± locale radiation

Bisphosphnates for bone mets

Prognosis = 70% 5 year survival, 10% for mets

42
Q

Childhood renal Ca name and Pres:

A

Wilms tumour - Nephroblastoma (primitive renal tubules)

Abdo mass + hameaturia

43
Q

AKI

  • Def
  • Effect
A

Acute decline in GFR: inc in Creatinine with/without oliguria(under 0.5 ml/kg/hr)/anuria (under 50ml/day)

Impaired clearance (urea/creatinine –> Azotaemia), imparted acid-base/electrolye/volume regulation

44
Q

AKI Causes

A

Pre (50%)

  • reduced perfusion (hypovolaemia, sepsis, haemorrhage, HF
  • Hepatorenal syndrome - GFR not responsive to fluids (liver failure = splanchnic dilation)
  • Renovascular disease (Bilateral stenosis) and drugs (NSAIDs, ACEi)

Intrinsic (30%)

  • Tubular necrosis (mainly sepsis - exogenous toxins, Abx and contrast also )
  • Glomerulonephritis
  • Interstitial nephritis

Post (20%)

  • Mechanical obstruction
  • calculi, BPH, Retention, pyelonephritis, retroperitoneal fibrosis, lymphoma
45
Q

Commonest pathology of AKIA

A

Acute tubular necrosis as a result of ischaemia (poor perfusion)

Hypoxaemia results in ROS, decreased ATP, cellular death

46
Q

Nephrotoxic drugs

Pre-renal

Intrarenal

Post renal

CANT DAMAG

A

Pre-renal

  • NSAIDS -> hypoperfusion
  • ACEI if compromised renal perfusion (e.g. renal artery stenosis) (DO NOT PRESCRIBE WITH NSAID)

Intrarenal

  • Glomerulonephritis: captopril, penicillamine, gold, penicillins, rifampicin
  • Interstitial nephritis: penicillins, cephalosporins, thiazide, furosemide, NSAID, rifampicin
  • ATN: aminoglycosides, ciclosporin

Post renal
- Anticholinergics (TCA) + alcohol -> retention

CANT DAMAG
Contrast, antibiotics (penicillin/ceph), NSAIDs, Therapeutic index (narrow), diuretics, ACEI, metformin, ARB, gentamicin/GOLD

47
Q

Staging AKI

- What is used

A

Creatinine: more than 3x baseline = stage 3

Urine output: les than 0.3mL/kg for 24 hours or anuria for 12hrs = Stage 3

48
Q

AKI

  • RFs
  • Pres
A

Older, underlying kidney disease, nephrotixics, DM, contrast, Liver failure + Ascites (Hepatorenal)

Decreased urine
Altered mental state (uraemia)
Peripheral oedema
Hypotension (suggests pre-renal)
Hypertension
49
Q

AKI investigaitons

A

U&E + Cr: elevated Cr, High serum K+, metabolic acidosis

Urine dip: infection (leukocytosis, nitrites), glomerular disease (blood/protein)

FBC: anaemia (blood loss), Leukocytosis (inf)

ECG: hyperkalaemia (inc PR, Wide QRS, Peaked T)

50
Q

AKI Tx approach

A

1) STOP nephrotoxics
2) ABCDE
3) Catheterise (monitor output)
4) VBG/ABG for K+ and ECG
5) USS KUB for obstruction
6) Urine dip (Inf, Blood/protein)
7) Dialysis for uraemia, acidosis, hyperkalaemia

51
Q

CKD

  • defa
  • epi
  • cause
  • pres
A

Evidence kidney damage (Prot/Haematuria)
+ reduced GFR
For over 3 months

10% of adult pop. Inc due to age.

DM and HTN commonly
Smoking
Obesity
AI disorders (focal segmental glomerulonephritis)

Majority of people are asymptomatic

52
Q

CKD

  • Tx
  • Complications
A

Glycaemic control

Increased risk of Cardiovascular disease -> main cause of death HF

53
Q 
CKD stages (%GFR)
1
2
3
4
5
A 
>90%
60-89%
59-30%
15-29%
< 15%

Remember: minus 30 then half twice
90, 60, 30, 15, under 15

54
Q

What is stage 5 CKD and what must be done?

A

This is end stage renal disease

Requires renal replacement therapy

  • Haemodialysis
  • Peritoneal dialysis
  • Tranplant
55
Q

CKD Aetiology (5 sections)

A

DM (50% ESRF)
- diabetic nephropathy due to glucose = albuminuria ± reduced GFR

HTN (30% ESFR)

  • Atherosclerotic disease = stenosis
  • HTN = renal scarring (glomerulosclerosis)

Nephrotic/nephritic syndromes

  • focal glomerulosclerosis
  • lupus nephritis
  • membranous nephropathy

PKD

Obstruction

  • Myelome
  • RCC
  • BPH
  • Stones
56
Q

Primary prevention CKD

Secondary prevention CKD

A

Good control DM (HbA1c under 7%) and BP ( under 140-90)
Smoking cessation
BMI under 27

As above, protein and salt restriction (control uraemia, prevent dialysis)

57
Q

CKD presentation

A

Hypertensive diabetic over 50

Fatigue (anaemia)
oedema (salt/water retention)
Nausea (uraemia) 
Arthralgia (If SLE)
Pruritus (uraemia)
58
Q

Uremic syndrome

  • Symp
  • Signs
A

Metallic taste
anorexia
N&V (gastritis)
seizures

Skin- grey, pruritus
Uraemic encephalopathy
Pericardial rub
Bone pain
Anaemia
59
Q

CKD complications

A

Anaemia (diminished EPO)

OSteodystrophy ( hypocalcaemia/phosphate retention due to Vit D def causes PTH release)

Cardiorenal syndrome (Na/H2O retention, volume expansion inc BP. inc pre-load due to renal hypoperfusion. HF & HTN as a result. These have knock on negative effect on kidneys)

Metabolic acidosis (unable to excrete acid)

Hyperkalaemia (unable to excrete as GFR declines)

Pulmonary oedema (fluid overload)

60
Q

CKD investigations

A

Serum Creatinine (elevated), if osteodystropthy - hyperphosphataemia, hypocalcaemia

eGFR (under 60% for significant

Urinalysis: haemorrhage/prot

Renal USS: obstruct/hydronephrosis, large kidney (RCC, Myeloma, amyloid)

FBC: anaemia

Antibodies: Autoantibodies (ANA), antibodies to strep antigens (glomerulonephritis)

61
Q

Management of CKD

A

Reversible causes: Obstruction, Nephrotixics

Glycaemic control

BP + CVD risk

  • ACEi/ARB2: target 140/90
  • statin, smoking, weight loss

Anaemia:
- Epoeitin alfa (stimulates SPO)

Bone disease:

  • Dietary inc in Ca, Calcitriol if low (active Vit D)
  • Phosphate binding drug (Calcium acetate)

Acidosis: oral sodium bicarb

Low protein and salt diet

62
Q

Renal replacement therapy

  • When used
  • Indicating factors
  • Inc risk to death
A

Severe AKI and ESRD (stage 5, eGFR < 15%)

Uraemia (pericarditis, gastritis, encephalopathy)

Pulmonary oedema (fluid retention)

Hyperkalaemia over 6.5% / Metabolic acidosis unresponsive to tx

Urea over 30

Each year dialysis inc risk of death by 6% (cardiovascular death)

63
Q

Haemodialysis

  • Mech
  • Access
  • Typical regimen
A

Blood passed over semipermeable membrane against dialysis fluid (opposite direction)
Blood meets less conc solution, small solutes can diffuse across conc grad.

AV fistula (bypassing capillary bed) Can also use a graft
Need Heparin infusion

Hospital 3X week for 4 hours OR home 5X 2-3 hours

64
Q

Haemodialysis complications;

A

Access: infection, thrombosis, aneurysm,

Hypotension

Air emboli

N&V

Anaphylaxis (sterilising agent)

Disequilibriation: restless, tremor, coma

65
Q

Who is harm-dialysis good for

A

Lives alone

Elderly

Cant have peritoneal dialysis

66
Q

Peritoneal dialysis

  • Mech
  • Access
A

Dialysate infused into peritoneal cavity.
Uses blood from peritoneal capillaries. altering osmolality of dialysate determines how much fluid removed

Catheter to peritoneum

67
Q

Peritoneal dialysis regimen

A

Continuous ambulatory with exchanges (last 20 min)
OR
Overnight

68
Q

Peritoneal dialysis

  • CI
  • Complications
  • Who does it suit
A

Intra-abdominal surgery/adhesions
Stoma
Obesity
Intestinal disease

Infection (peritonitis, catheter)
Catheter block/leak
Constipation
Hyperglycaemia + weight gain
Hernia

Young, indépendant, lack of healthcare access

69
Q

Renal transplant

  • Advantages
  • Types
  • Location
A

Inc survival, QoL, Economic advantage in long term, enable pregnancy (Kidney disease/Dialysis affects eggs and menstruation)

Cadaveric (90%), living donor (10%)

Right iliac fossa

70
Q

Matching a renal transplant (3 things)

A

ABO group and crossmatch

HLA

  • On 6 loci
  • A and B (X2) present Ag to CD8 (cytotoxic) cell
  • DR (X2) present to CD4 (Th) cell

Antibody screening

71
Q

Immunosuppression in kidney transplant

A

Induction (at time): Basiliximab + IV methylprednisolone

Maintain: Prednisolone, Calcineurin inhibition’s (Block t-cell activation e.g. tacrolimus/ciclosporin), antimetabolites (azathioprine)

72
Q

CI for renal transplant

A

Cancer
Active infection
Uncontrolled Ischaemic heart disease
AIDs with opportunistic infection

73
Q

Renal transplant Risks

A

Surgery: Infection, DVT, pain

Immunosuppression:
BM suppression, Ca (Skin, Lymphoma), infection

CV disease (HTN, dyslipidemia)

Rejection:

  • hyper acute:mins, cross match error
  • Accelerated: days, T-cell. fever swollen kidney, inc Cr. Give IV steroids
  • Acute cellular: weeks (25%), fluid retention, inc BP and Cr. Give high dose IV steroids
  • Chronic: years, gradual Cr rise and proteinuria, HTN. fibrosis and atrophy on graft biopsy. Not responsive to immunosuppression will need RRT again
74
Q

Renal tranplant prognosis

A

Cadaver
1yr 90%,
10yr 65%

Live
1yr 96%,
10yr 80%

75
Q

Glomerular disease classifications

A

Nephrotic:

  • Proteinuria
  • Peripheral oedema
  • In children minimal change disease commonest - Steroids
  • Hypoalbuminaemia and hyperlipidaemia (liver synthetic compensation)

Nephritic:

  • Inflamation of glomeruli = Oliguria + Hematuria (cola coloured)
  • Berger’s disease (IgA nephropathy) commonest cause
76
Q

Glomerulonephritis

  • def
  • complication
  • common type
A

Glomerular injury due to immune mediated damage of glomerular capillaries and basement membrane (e.g. Berger’s IgA nephropathy, SLE)

3rd most common cause ESRD

Focal segmental glomerulonephritis

77
Q

Causes of Glomerulonephritis

Systemic disease
Infection
Drugs
Other

A

SLE, RA, Goodpastures, Wegners, HSP, HUS, Scleroderma

Group A strep (pyogenes) - immune complex, Hep B/C

Penicillamine (DMARD and used in Wilsons to bind copper), Ciclosporin, NSAIDs, Gold

DM, HTN, Lunc/colorectal cancer

78
Q

Glomerulonephritis pathophysiology

A

Immune mediated injury due to 2 possible mech

1) cellular immune response: Leukocyte and macrophage infiltration (focal glomerulosclerosis)

2) immune complex formation and deposition + complement activation in glomerulus
- antibodies may bind with autoantigens e.g. in anti basement membrane disease
- extrinsic antigens bound to antibodies may deposit e.g. post infection
- complement, cytokine and growth factor activation = structural and functional changes

Non-immune: Hyperglycaemia, high intraglomerular pressure (HTN)

79
Q

Nephrotic Vs Nephritic

A

Nephrotic = non-proliferative disease

  • Proteinuria,
  • hypoalbuminaemia,
  • peripheral oedema,
  • hyperlipidaemia

Nephritic = proliferative disease

  • Oliguria/AKI
  • HTN
  • Haematuria (Red cells and casts)
80
Q

Causes of Nephrotic syndrome

A

Deposition disease (Amyloid, light chain deposition - myeloma = Bence jones)

Minimal change disease

Other:
Focal, segmental, membranous, mebranoproliferative

81
Q

Causes of Nephritic syndrome:

A 
IgA Nephropathy (Berger's)
Postinfective

Vasculitis

Anti-GBM

82
Q

Nephrotic syndrome
- Children: cause, Tx

  • Young adults: Cause
A

Minimal change
Light microscopy normal, immunoflourscence = no deposition

Steroids (Prednisalone)

Focal segmental glomerulonephritis: idiopathic or secondary to HIV.
Light micro shows focal areas of sclerosis

83
Q

Ddx nephrotic syndrome

A

Other diseases causing Peripheral oedema

  • Congestive heart failure
  • Liver disease (Dec albumin)
84
Q

Nephrotic syndrome complications

A

Infection: IgG loss or secondary to steroids

Hypercholesterolaemia: inc hepatic synthesis of lipoproteins

Hypervoleamia: Dec in GFR, oedema

HTN: GFR impaired (not as much as nephritic)

85
Q

Nephritic syndrome

  • def
  • most common
  • Other
A

Acute kidney injury with deterioration of function

Most common = Buergers
- Macroscopic haematuria 2due to IgA deposition

Membranoproliferative: secondary to SLE causes thickening of GBM

Post infective: immune complex post Group A strep

Rapidly progressive (crescenteric)

  • Vasculitis: Wegner’s (cANCA), microscopic polyangitis (pANCA)
  • AntiGBM
86
Q

Glomerulonephritis

  • Pres
  • other symp
A

Haematuria + Oedema + HTN + Oliguria

weight loss (systemic), nausea (vasculitic), fever (Infection), arthralgia (Vasculitic), haemoptysis (antiGBM)

87
Q

Glomerulonephritis investigatons

A

U&E, Cr - GFR normal or reduced

Urinalysis: haematuria, proteinuria, RBC casts

ESR - vasculitis
Complement - low in immune complex
antiGBM antibody
ANA - SLE
Renal biopsy
88
Q

Glomerulonephritis management

A

Abx if post strep (phenoxymethylpenicillin)

moderate: haematuria + proteinuria + low GFR
- Reduce proteinuria: ACEi + furosemide + prednisolone
- immunosuppressive: cyclophosphamide

Rapidly progressive:

  • antiGBM: plasma exchange + IV methylprednisolone + IV cyclophosphamide
  • Lupus nephritis: IV methylpred + Cyclophosphamide
89
Q

PKD

  • Def
  • Forms
  • Characterised by
A

inherited cystic disease of kidneys

ADPKD (most common)
ARPKD

Renal cysts, intracranial aneurysms, aortic root dilatation and aneurysms, mitral prolapse, extra-renal cysts

90
Q

PKD complications

A

HTN, CV morbidity (aneurysms rupture), CKD, End stage renal disease

91
Q

Genes in PKD

A

Autosomal Dominant or recessive

Two PKD loci
- PKD1 - 85% ESRF at 50
PKD2 - 15% ESRF at 50

92
Q

PKD pathophysiology

A

POlycystin 1 and 2 make protein complex involved in Ca regulation

Disruption affects cell signalling and inc proliferation

cAMP activation (Ca) and cAMP mediated cysts expansion/fluid secretion

Cysts form in tubular portion of nephron compress renal architecture and infrarenal vasculature (interstitial fibrosis and tubular atrophy

93
Q

ARPKD

A

More severe form

High mortality

Neonated often present with large kidneys, renal cysts, hepatic cysts and fibrosis

15 year survival is low (50-80%)

94
Q

PKD presentation

A

FH or PKD/ESRD or Haemorrhagic stroke

Lumbar pain (females), haematuria (males), HTN at 25-30yr (renal USS to screen)
Palpable kidneys
headache (aneurysms)
Hepatomegaly (Liver)

95
Q

PKD extra renal cyst locations

A

Liver (80%)
Pancreas (10%)
Seminal vesicles (40%)
Brain (10%)

96
Q

PKD investigations

A

Renal USS for cysts

Genetic testing (PKD1 or PKD2 mutation)

CT abdo pelvis (kidney and extra renal cysts)

Urinalysis (protein), ECG (LVH - HTN), ECH) (aortic root dilatation)

MR angio (aneurysm screen)

SCREEN FAMILY Kidneys and SAH (MR angio)

97
Q

PKD management

A

UTI/infected cyst: Ciprofloxacin

PAin: analgesia (para, naproxen) ± laparoscopic cystectomy ± nephrectomy

ESRD: RRT (transplant or dialysis)

Target cell proliferation ( somatostatin (GH)

Intracranial: neurosurgical + nimodipine (CCB helps improve blood flow after aneurysm)

Genetic counselling

98
Q

Types of Post Strep Glomerulonephritis (giving heamaturia)

A

IgA (1-2 days post URTI)

Immune complex (1-2 weeks post-URTI)

99
Q

4 things in renal failure (Aki)

A

Uraemia
Acidosis
Hyperkalaemia
Fluid overload

100
Q

Fluid overload in AKI

A

Pulmonary oedema (CXR)

101
Q

Aki and glomerulonephritis

A

Two types of glomerulonephritis (phrotic/phritic)

Both are cause of AKI

Final (26 decks)

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