Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Medicine > Renal Medicine > Flashcards

Renal Medicine Flashcards

1
Q

What features describe Stage 1 CKD?

A

eGFR > 90mL/min with evidence of renal damage e.g. proteinuria, haematuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What features describe Stage 2 CKD?

A

eGFR = 60-89mL/min with evidence of renal damage e.g. proteinuria, haematuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What features describe Stage 3A CKD?

A

eGFR = 45-59mL/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What features describe Stage 3B CKD?

A

eGFR = 30-44mL/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What features describe Stage 4 CKD?

A

eGFR = 15-29mL/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What features describe Stage 5 CKD?

A

eGFR less than 15mL/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What features describe Stage 1 AKI?

A
  • Serum Creatinine increase >26umol/L in 48h
  • OR increase creatinine 1.5 x baseline
  • OR urine output less than 0.5mL/kg/hr for at least 6 consecutive hours
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What features describe Stage 2 AKI?

A
  • Serum Creatinine increase 2-2.9 x baseline

- urine output less than 0.5mL/kg/hr for at least 12hr

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What features describe Stage 3 AKI?

A
  • Serum Creatinine increase >3 x baseline
  • OR creatinine over 354umol/L
  • OR urine output less than 0.3mL/Kg/Hr for at least 24hr
  • OR anuria for 12h
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are some risk factors for developing AKI?

A

Age >75, CKD, Cardiac Failure, peripheral vascular disease, chronic liver failure, diabetes, drugs, sepsis, poor fluid intake/increased losses, history of urinary symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe IgA Nephropathy and treatment

A

a.k.a. Berger’s disease most common cause of glomerulonephritis worldwide due to IgA complex depositon.

Presentation: young male, recurrent episodes of macroscopic haematuria, few days after URTI

Rx: Steroids + cyclophosphamide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe Post-streptococcal glomerulonephritis, it’s symptoms, treatment

A

a.k. proliferative GN
Immune complex deposition that occurs 7-14days post strep infection most commonly in children.
Strep antigens deposited on glomerulus –>host response and immune complex formation

Features: Headache, malaise, haematuria, nephritic syndrome, hypertension, low C3, raised ASO (AntiStreptolysin O) titre

Supportive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe Alport’s syndrome

A

Alport’s syndrome is an inherited disorder of type IV collagen resulting in abnormal glomerular basement membrane.

Features:
microscopic haematuria
progressive renal failure
bilateral sensorineural deafness
lenticonus: protrusion of the lens surface into the anterior chamber
retinitis pigmentosa
renal biopsy: splitting of lamina densa seen on electron microscopy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Define Nephrotic Syndrome, its causes, complications and management

A

Triad of Proteinuria >3.5g/24h (ACR >250mg/mmol), hypoalbuminaemia and oedema

Primary causes: Minimal change disease, membranous nephropathy, focal segmental glomerulosclerosis, mesangiocapillary glomerulonephritis
Secondary causes: Hepatitis B/C, SLE, diabetic nephropathy, amyloidosis, paraneoplastic, drugs (NSAIDs, penicillamine, anti-TNF, gold)

Complications: susceptibility to infection, thromboembolism, hyperlipidaemia

Management:

  • Reduce oedema (Loop diuretic),
  • Reduce proteinuria (ACE-inhibitor, Angiotensin-Receptor Blocker)
  • Reduce risk of complications (anticoagulate, statin), and Treat underlying cause.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe Minimal Change Disease and its treatment.

A

Commonest cause of nephrotic syndrome in children

Biopsy normal under light microscopy.

T-cell and cytokine mediated damaged to GBM leads to polyanion loss and the resultant reduction of electrostatic charge increased glomerular permeability to serum albumin.

Treatment:

  • Spontaneous remission is possible, and remission can be induced with steroid therapy but may relapse (steroid-dependent) or be resistant (Steroid Resistant).
  • Steroid-resistant disease or steroid-dependent disease can be treated with cyclophosphamide or tacrolimus. 1% progress to ESRF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe membranous nephropathy

A

Second most common cause of nephrotic syndrome in adults accounting for 20-30%.

primary or secondary due to malignancy, hepatitis B, drugs (NSAIDs, Gold, Penicillamine) Autoimmune (SLE, Thyroid).

Biopsy shows diffusely thickened GBM with subepithelial deposits of IgG and C3 on immunofluorence. Treatment involves managing nephrotic syndrome.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe mesangiocapillary glomerulonephritis

A

May be immune complex mediated or complement mediated and may be due to underlying cause such as Hepatitis C, SLE, monoclonal gammaglobulinopathies.

Biopsy shows mesangial and endocapillary proliferation, thickened GBM and double contouring (tramline) of the capillary walls.

Treat underlying cause and nephortic syndrome. prognosis poor when no underlying cause is found and in patients with ESRF if can reoccur in transplants.

18
Q

Describe focal segmental glomerulosclerosis (FSGS)

A

Most common cause of nephrotic syndrome in adults.

May be primary (idiopathic) or secondary (Vesicoureteric reflux, IgA nephropathy, vasculitis, Alport’s syndrome, sickle-cell disease, heroin use).

Biopsy shows segmental glomerular scarring and IgM and C3 deposits on immunofluorence.

10% remit spontaneously, may respond to corticosteroids or cyclophosphamide if resistant. Can progress to ESRF and reoccur ~20% of transplants.

19
Q

Describe Rhabdomyolysis, its causes and clinical features.

A

Rapid muscle breakdown with release of K+, Phosphate, myoglobin, urate, and creatine kinase. This leads to hyperkalaemia and AKI due to renal tubule obstruction by myoglobin.

Causes include trauma (burns, crush injury, uncontrolled seizures), Drugs and toxins (statins, alcohol, ectasy, heroin, neuroleptic malingant syndrome), metabolic (hypokalaemia, myositis) and inheritied muscle disorders (duschenne’s muscular dystrophy, McArdle’s disease)

Clinical features: red-brown urine (visible myoglobinuria), muscle pain, hyperkalaemia, Increased phosphate, plasma CK >1000iU/L, hypocalcaemia, hyperuricaemia.

20
Q

Name some nephrotoxic drugs

A

NSAIDs, antimicrobials (genatmicin, sulfonamides, penicillins, rifampicin, amphotericin, aciclovir), anticonvulsants (lamotrigine, valproate, phenytoin), omperazole, furosemide, thiazides, ace-inhibitors, ARBs, cimetidine, lithium, iron, cisplatin, radiocontrast.

21
Q

What are some causes of AKI?

A

Pre-renal: (40-70%) due to renal hypoperfusion e.g. hypotension, renal artery stenosis

Intrinsic renal: (10-50%) tubular (acute tubular necrosis is the commonest, also myeloma, ethylene glycol poisoning, hyperuricaemia, hypercalceamia) glomerular (autoimmune e,g, SLE, Henoch-scholein purpura) Interstitial (infilitration from infection, tumour lysis syndrome) Vascular (vasculitis, HUS/ TTP)

Post-renal: (10-25%) caused by urinary tract obstruction e.g. stones, malignancy (compression

22
Q

What are the complications of AKI?

A

Hyperkalaemia, pulmonary oedema, uraemia, acidaemia,

23
Q

Describe Haemolytic Uraemic Syndrome (HUS)

A

Endothelial damage commonly (90%) from E.coli strain O157 leads to thrombosis, platelet consumption and fibrin strand deposition mainly in renal microvasculature. Strands cause mechanical destruction of RBC’s giving triad of haemolysis, thrombocytopenia and AKI. It is most common cause of AKI in children. Clinical features include abdominal pain, bloody diarrhoea and AKI.

24
Q

What are the causes of CKD?

A

Diabetes (20%), hypertension, glomerulonephritis (commonly IgA nephropathy also SLE, Vasculitis), Unknown

25
Q

Describe Acute Tubular Necrosis (ATN)

A

Most common cause of AKI, characterised by death of tbular epithelial cells due to ischaemia most commonly caused by hypotension or nephrotoxic drugs.

The presence of “muddy brown casts” of epithelial cells found in the urine during urinalysis is pathognomonic for ATN

26
Q

Describe Thrombotic Thrombocytopenic Purpura (TTP)

A

Overlap with HUS, patients are Thrombocytopenic and have microangiopathic haemolytic anaemia. Other features include AKI, CNS involvement, fever. Due to an genetic or acquired deficiency of protease ADAMTS13 which normally cleaves VonWillebrand multimers

Do not infuse platelets

27
Q

Describe transplant rejection

A

Acute (<6 months): increase serum creatinine, fever, graft pain. Immune cell infiltrate and tubular damage.
Rx - high dose IV methylprednisolone. if resistant - anti-thymocyte globulin, OKT3

Chronic (>6 months): interstitial fibrosis and tubular atrophy. Gradual increase in creatinine and proteinuria.
Rx - general management of chronic renal failure (not responsive to immunosuppression)

28
Q

Describe renal biopsy, its indication, pre procedure checks, contraindications and complications

A

Patients lay on their front, local anaethetic used and core biopsy taken. Bed rest on back for minimum of 6h

Indications:

  • unexplained AKI or CKD
  • acute nephritic syndrome
  • unexplained proteinuria or haematuria
  • suspected transplant rejection
  • systemic disease associated with kidney dysfunction

Pre procedure check: FBC, clotting, group and save. obtain written consent. Ultrasound to delineate anatomy (Horseshoe kidney?, two kidney? Size?). Stop anticoagulants (asprin 1 wk, wafarin 3 days, LMWH 1 day)

Contraindications:

  • abnormal clotting
  • hypertension greater than 160/90mmHg
  • single kidney
  • CKD with small kidneys (less than 9cm)
  • uncooperative patient
  • horseshoe kidney
  • renal neoplasms.

Complications:

  • Bleeding, macroscopic haematuria occurs in 1/10
  • Bleeding requiring transfusion in 1/100
  • nephrectomy rare
29
Q

What are the indications of dialysis?

A
  • hyperkalaemia unresponsive to medical treatment or in an oliguric patient
  • Pulmonary oedema unresponsive to medical treatment
  • uraemic complications such as pericarditis or encephalopathy
  • severe metabolic acidosis unresponsive to treatment (pH
30
Q

Describe Renal tubular acidosis, its types, and treatment.

A

Is a metabolic acidosis due to impaired acid secretion by the kidney. There is a hyperchloraemic metabolic acidosis with normal anion gap.

Types: There are 4 types and type 3 is a combination of type 1 and 2.

  • Type 1 (distal) RTA is due to an inability to excrete H+ and generate acidic urine in the distal tubule.
  • Type 2 (proximal) is due to a ‘bicarbonate leak’ a defect in HCO3 reabsorption in the proximal tubule resulting in excess HCO3 in the urine.
  • Type 4 (hyperkalaemic) is due to hyporeninaemic hypoaldosteronism. hypoaldosteronism causes hyperkalaemia and acidosis.

Treatment: is with bicarbonate.

31
Q

Describe nephritic syndrome and its causes.

A

Nephritic syndrome includes haematuria, proteinuria, hypertension and ureamia.

Primary causes include IgA nephropathy and mesangiocapillary glomerulonephritis.

Secondary causes include post-streptococcal, vasculitis, SLE, Goodpastures, cryoglobulinaemia.

32
Q

Describe Hyperkalaemia, its signs, symptoms, causes and treatment

A

Plasma potassium >5.5mmol/L, increased potassium leads to myocardial hyperexcitability leading to ventricular fibrillation and cardiac arrest.

Signs + symptoms: Fast irregular pulse, chest pain, weakness, palpitations, light-headedness.
ECG: tall tented T waves, small p waves, wide QRS, VF.

Causes:
Artefact - haemolysis, contamination, thrombocythaemia, delayed analysis
Excessive intake - oral,/parenteral, massive transfusion
Transcellular movement (ICF -> ECF) - metabolic acidosis (DM), insulin storage, rhabdomyolysis, burns
Decreased excretion: oliguric renal failure, K+ sparing diuretics, addison’s disease, drugs (e.g. ACEi, NSAIDs, ARB, Suxamethonium)

Treatment:
Monitor ECG
If K+ > 6.5 mmol/l or if there are ECG changes:
- 10ml 10% calcium gluconate IV over 2 mins
- 50ml 50% glucose + 10U insulin (actrapid)
- salbutamol 5mg nebs
- Calcium resonium 15g PO or 30g PR
- Haemofiltration

If non-urgent - treat underlying cause, review medications; give calcium resonium 15g/8hr PO

33
Q

Describe Syndrome of Inappropriate ADH secretion (SIADH), it’s causes, and management.

A

A cause of hyponatraemia and decreased Urine output, SIADH consists of:
-concentrated urine (Na+ > 20mmol/L, osmalility >100mosmol/kg)
-hyponatraemia (plasma Na less than 125mmol/mL)
-low plasma osmolality (less than 260mosmol/kg)
in the absence of hypovolaemia, oedema or diuretics

Causes:

  • malignancy: Lung small cell, pancreas, prostate, thymus, lymphoma
  • CNS disorders: Menigoencephalitis, abscess, stroke, subarachnoid or subdural haemorrhage, head injury, neurosurgery, guillain-barre, SLE, Vasculitis
  • Chest disease: TB, pneumonia, abscess, aspergillosis, small cell lung cancer
  • Endocrine: Hypothyroidism
  • Drugs: Sulfonylureas, SSRIs, tricyclics, carbamazepine, vincristine, cyclophosphamide.
  • Other: Acute intermittent porphyria, trauma, abdominal or thoracic surgery, symptomatic HIV.

Management:
-identify and treat the cause
- fluid restrict
Consider salt +/- loop diuretics

34
Q

What are the causes of Hyperuricaemia?

A

Drugs: Cytotoxics, Thiazides, Loop Diurectics, pyrazinamide

Increased Cell Turnover : lymphoma, leukaemia, psoriasis, haemolysis, rhabdomyolysis, tumour lysis syndrome

Reduced Excretion: primary gout, chronic kidney disease, lead nephropathy, hyperparathyroidism, pre-eclampsia

35
Q

Describe Acute Urinary Retention, its causes, symptoms, and management

A

Causes: prostatic obstruction (usual cause in males), urethral strictures, anticholinergics, alcohol, constipation, post-op, infection, neurological (cauda equina syndrome), carcinoma.

Symptoms: Tender bladder, anuria, dull percussion of bladder.

Management:

  • MSU, U+E, FBC, and PSA to help identify cause.
  • Conservative management: tricks to aid voiding such as analgesia, privacy on hospital wards, ambulation, standing to void, voiding to sound of running taps or in a hot bath.
  • Other wise Catheterise and start an alpha-blocker e.g. Tamulosin.
  • Monitor for post-obstructive diuresis, in acute phase after relief of the obstruction, the kidneys produce a lot of urine, match input to output.
  • TWOC
36
Q

Describe Hypokalaemia, it’s signs and symptoms, causes, and management

A

If K+ less than 3.5mmol/L

Signs and Symptoms: Muscle weakness, hypotonia, hyporeflexia, cramps, tetany, palpitations, light-headedness (arrhytmias), constipation
ECG - small/inverted T waves, prominent U waves, long PR interval, depressed ST segments

Causes:
- GI losses: diarrhoea, vomiting, purgative and liquorice abuse, pyloric stenosis, rectal villous adenoma, intestinal fistula
- Renal losses: Conn’s syndrome, diuretics
- Redistribution: Cushing’s/steroids/ACTH, B-agonist, alkalosis
Othrs: Renal tubular acidosis 1 +2, hypomagnesaemia

Management:

  • mild (>2.5, asymptomatic): oral K+ supplements (Sando K 2 tabs/8hr). Review after 3 days
  • Severe (<2.5, symptomatic): IV potassium (max 10mmol/hr)
37
Q

Describe Urinary Tract Calculi (aka kidney stones, nephrolithiasis), it’s presentation, investigations and management.

A

Stones form in collecting ducts and may be deposited anywhere from the renal pelvis to the urethra.

Signs and symptoms:
Asymptomatic
Renal colic (severe waxing and waning loin pain radiating to the groin or thigh, with fever or vomiting),
Renal obstruction (loin pain),
UTI can co-exist (burning sensation, increased urinary frequency), and pyelonephritis (fevers, rigours, loin pain, nausea and vomiting).

Investigations:

  • Bloods: FBC, U+E, Ca2+, PO43-, glucose, bicarbonate, urate.
  • Urinalysis
  • MSU: MC+S
  • Imaging: USS, Non-contrast CT (IVU, KUB Xray)

Management:
-Analgesia e.g. Diclofenac 75mg IV/IM or 100mg PR
-Antibiotics e,g, Cefuroxime 1.5mg/8h IV or gentamicin if infection
-Stones <5mm pass spontaneously, increase fluid intake
-Stones >5mm or pain not resolving require
medical expulsion therapy with nifedipine 10mg/8h or tamsulosin 0.4mg/d
extracorporeal shockwave lithotripsy (SEs renal injury, may also cause hypertension and DM.
Percutaneous nephrolithotomy

38
Q

Describe Polycystic Kidney disease, symptoms, and management.

A

Autosomal dominant, 85% have a mutation in PKD1 on chromosome 16 and 15% in PKD2 in chromosome 4. The first type present with renal failure earlier.

Symptoms:
Renal enlargement with cysts causing abdominal pain +/- haematuria, and hypertension.
Extrarenal symptoms: liver cysts, SAH (berry aneurysms), mitral valve prolapse, ovarian cysts, diverticular disease.

Management:
- General: Increase water intake, decrease Na+, decrease caffeine. Monitor U+E and BP (aim <130/80)
Genetic counselling. MRA screening
- Medical: Rx hypertension agreesively. Rx infection.
- Surgical: if pain, recurrent bleeds or infection - laparoscopic cyst removal or nephrectomy

For ESRF - Dialysis/ transplantation

39
Q

Describe Bartter’s syndrome and its symptoms.

A

An autosomal recessive cause of severe Hypokalaemia due to defective chloride absorption at the NKCC2 in the ascending loop of Henle. It is Socrates with normotension unlike other causes of Hypokalaemia such as Conn’s, Cushings and Liddles.

Symptoms: Polyhydraminos in utero, Failure to thrive, Polyuria, polydipsia, Hypokalaemia, normotension, weakness.

40
Q

Types of Stones from urinary tract calculi

A

Calcium oxalate (75%) - radio-opaque
Magnesium ammonium phosphate (Triple phosphate/struvite) (15) - UTI - proteus, staghorn calculi, radio-opaque
Urate - hyperuricaemia, smooth,brown, radiolUcent
Brushite
Cysteine - Renal tubular defects, yellow, crystalline, semi-opaque
Hydroxyapatite
Calcium phosphate
Mixed

Medicine (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions