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Meded Flashcards 2020 > renal > Flashcards

renal Flashcards

1
Q

What is the function of the kidney?

A
  • •Regulation of blood volume
  • •Regulation of blood pressure
  • •Acid-base balance
  • •Electrolyte balance
  • •Production of Red blood cells
  • •Synthesis of Vitamin D – Bone metabolism
  • •Excretion of water-soluble waste products – Filter
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2
Q

What are the different stages of AKI?

A

Stage 1: creatinine rise of 1.5x compared to baseline or urine output <0.5 ml/kg/hour for 6 hours.

Stage 2: creatinine rise of 2x compared to baseline or urine output <0.5 ml/kg/hour for 12 hours.

Stage 3: creatinine rise of 3x

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3
Q

How does the patient present in AKI?

A

Symptoms

  • •Depends on underlying CAUSE
  • •Oliguria/anuria
  • •NOTE: abrupt anuria suggests post-renal obstruction
  • •Nausea/vomiting
  • •Dehydration
  • •Confusion

Signs

  • •Hypertension
  • •Distended bladder
  • •Dehydration - postural hypotension
  • •Fluid overload (in heart failure, cirrhosis, nephrotic syndrome) - raised JVP, pulmonary and peripheral oedema
  • •Pallor, rash, bruising (vascular disease)
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4
Q

What is the mechanism behind pre renal failure?

What are the complication?

A

Due to Renal Hypoperfusion, most common causes are hypotension due to sepsis and hypovolaemia from fluid loss.

No blood to kidney = no pee = AKI

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5
Q

Haemolytic uraemic syndome

What is it charactrised by?

What is the pathophysiology

WHat infection precedes it usually

What is the treatment

A

What is it charactrised by?

  1. Progressive renal failure - Kidneys
  2. Microangiopathic haemolytic anaemia (MAHA) – Blood
  3. ↓ Platelets - Blood

What is the pathophysiology?

  1. Gastroenteritis (E.coli 90%) -> toxin
  2. Endothelial damage
  3. Thrombosis, platelet consumption + fibrin strand deposition → ↓ Platelets
  4. Destruction of RBCs – schistocytes, ↓ Hb

What infection precedes it usually?

E coli

What is the treatment?

Mainly supportive

  • dialysis
  • NO antibiotics
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6
Q

How do treat Diabetic nephropathy?

A
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7
Q

What is the spectrum of Glomerulonephritis?

Name one important fact about them and where thy are on the spectrum

A

NEPHROTIC:

Primary:

Minimal change disease- in children - treat with corticosteoids

Membranous Nephropathy/Glomerulonephritis- commonest type in adults- subepithelial immune complex deposits

Focal segmental glomerulosclerosis- sclerosing of glomeruli in segments- IgM and complement deposition

Membranoproliferative glomerulonephritis- really rare

Secondary to Systemic Disease

  1. DM- 5 stages, Stage 1 hyperfiltration, Stage 2 silent, Stage 3 microalbuminuria, Stage 4 persistant protenuria with hypertension, Stage 5 end stage renal disease
  2. SLE- SOAP BRAIN MD
  3. Amyloidosis

Nephritic

  • IgA Nephropathy / Berger’s Disease- commonest -macroscopic haematuria few days after Upper respiratory tract infecton- IgA & C3 depostition
  • Post-streptococcal glomerulonephritis- 1-2 weeks after sore throat or skin infection- common in children
  • Crescentic/ Rapidly progressive glomerulonephritis
    • Type 1: Anti-GBM- Goodpasture syndrome- Anti GBM antibodies against type 4 collagen- affects long and kidney
    • Type 2- Immune complex deposition
    • Type 3 Pauci immune
  • Thin BM Disease - Autosomal dominant- thinning GBM by mutatio of type 4 collagen alpha 4 chain
  • Alport’s Syndrome- X- linked recessive 4 collagen alpha 5 chain, EAR sensory neural deafness, EYE, lense dislocation - cataract
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8
Q

TTP

What are t?

What is the pathophysiology?

What is the pentad?

A

What is it?

What is the pathophysiology?

  • Deficiency of protease (ADAMTS13) that cleaves cleave vWF à
  • Large vWF multimers form à
  • Platelet aggregation & fibrin deposition
  • Microthrombi

What is the pentad?

ADAMTS-13

NO Antibody
Decreased platelet
AKI
MAHA
Temperature
Swinging CNS (Seizures, hemiparesis, ↓ consciousness,↓ vision)
13- (von willebrandt 13 letters- so can’t break that down)

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9
Q

how do you approach an AKI

A
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10
Q

What does this ECG show?

How would you treat this

A
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11
Q

GLomerulonephritis table MEDED- less extensive than other flashcards

A
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12
Q

Fill in the table

A
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13
Q

What are causes of an AKI? annotate the diagram

A
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14
Q

What could causes these findings on a urine dip?

A
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15
Q

What are the differences between nephrotic and nephritis syndrome

A
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16
Q

What is this?

A

Polycystic ovary syndrome

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17
Q

SBA1

A

A

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18
Q

SBA 2

A

E

Diclofenac is a strong non-steroidal anti-inflammatory drug (NSAID) that is usually prescribed for muscular injury and renal colic. NSAIDs inhibit the production of prostaglandins, which are essential in maintaining renal perfusion. NSAIDs are therefore nephrotoxic and should be avoided in patients with known renal disease and in those at risk of renal disease, e.g. elderly people. Long-term use of NSAIDs may lead to analgesic nephropathy and chronic renal failure.

Analgesic nephropathy is injury to the kidneys caused by analgesic medications such as aspirin, phenacetin, and paracetamol. The term usually refers to damage induced by excessive use of combinations of these medications, especially combinations that include phenacetin. It may also be used to describe kidney injury from any single analgesic medication.

The specific kidney injuries induced by analgesics are renal papillary necrosis and chronic interstitial nephritis. They appear to result from decreased blood flow to the kidney, rapid consumption of antioxidants, and subsequent oxidative damage to the kidney. This kidney damage may lead to progressive chronic kidney failure, abnormal urinalysis results, high blood pressure, and anemia. A small proportion of individuals with analgesic nephropathy may develop end-stage kidney disease.

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19
Q

SBA3

A

D

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20
Q

SBA 3

A

E

Goodpasture’s syndrome is a rare condition in which autoantibodies are formed against the glomerular basement membrane and the alveolar membrane. The antibodies trigger a type II hypersensitivity reaction that causes renal failure, pulmonary haemorrhage and haemoptysis. The condition is usually diagnosed by the detection of anti-glomerular basement membrane antibody (anti- GBM) in the serum and via renal biopsy. The biopsy often shows focal or diffuse crescentic glomerulonephritis. Immunofluorescence may demonstrate linear deposition of IgG antibodies and complement (C3) on the glomerular basement membrane. Goodpasture’s syndrome is usually treated aggressively with plasmapheresis, corticosteroids and immunosuppression.

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21
Q
A

B.

Membranous glomerulonephritis is the most common cause of nephrotic syndrome in adults. In this condition, immune complexes are formed when circulating antibodies bind to basement membrane antigens or antigens deposited in the glomerulus from the circulation. The immune complexes activate an immunological response that involves the complement cascade. This response damages the glomerular basement membrane, making it more leaky to protein

Rapidly progressive glomerulonephritis – aka crescentic glomerulonephritis

3 main cause

  • Immune complex-associated (SLE, IgA, post-infectious glomerulonephritis)
  • Anti-GBM disease
  • Pauci-immune crescentic glomerulonephritis (ANCA)
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22
Q

What is the triad of the nephrotic syndrome?

What are other symptoms

A
  1. proteinuria
  2. low serum albumine
  3. oedema

Liver tries to increase the production of albumin and at the same time produces more lipids (hyperlipidaemia)

loss of antithrombin 3 and hypogammaglobuliaemia leads to hypercoagulable state

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23
Q

What are common condition in adult and child that lead to a nephrotic syndrome

A

adults: membranous glomerulonephritis OR DM

children; minimal change glomerulonephritis

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24
Q

What is the nephritic syndrome triad

A
  1. Haematuria
  2. hypertenison
  3. oedema

CAST cells prove haematuria is glomerular

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25
**_What are investigation and management of Glomerulonephritis?_**
**_Investigations:_** * Bloods – FBC, U&Es, CRP, Complement, Autoantibodies * Urine * Imaging – renal US +/- renal biopsy **_Management:_** * Refer specialist * BP management – \<130/80 * ACE-I or ARB – reduce proteinuria and preserve renal function * Steroids/immunosuppression * Treat underlying cause
26
What is the most common renal cause of AKI?
acute tubular necrosis
27
What can renal tubular injury be due to?
ischaemia nephrotoxic agents
28
What are exogenous and endogenous causes of acute tubular necrosis?
**_Exogenous:_** * **Drugs**: NSAIDs, Aminoglycosides, amphotericin b, contrast media, calcineurin inhibitors, cisplatin etc. **_Endogenous:_** * myoglobinaemia (rhabdomyolysis), * haemaglobinuria * crystals * myeloma
29
**What is rhabdomyolysis?** **What is the pathophysiology** **What is the presentation** **What are the investiagtions**
**What is rhabdomyolysis?** Skeletal muscle death **What is the pathophysiology** release of myoglobin, potassium and creatinine kinase (CK), obstruction of renal tubules - acute tubular necrosis **What is the presentation?** Muscle pain and swelling, dark urine (myoglobin) **What are the investiagtions** •Hyperkalaemia, High CK
30
What is the pathophysiology of Acute tubular necrosis due to ischaemia? What are the 3 phases?
**What is the pathophysiology of Acute tubular necrosis due to ischaemia?** 1. Ischaemia \> 2. Tubular cell injury \> 3. Necrosis \> 4. Obstruction of tubule by debris \> 5. ↓GFR **What are the 3 phases**? 3 phases: 1. INITIATION –acute ↓ GFR + ↑ Cr + ↑urea 2. MAINTENANCE – sustained ↓ GFR (~1-2w) à Cr + urea ↑ 3. RECOVERY – tubular function regenerates à ↑urine volume + gradual ↓ urea + Cr
31
**What cancer can cause acute tubular necrosis?** **What is the pathophysiology?** **What are the clinical features?**
**What cancer can cause acute tubular necrosis?** Malignant disease of bone marrow plasma cells which results in a clonal expansion of plasma cells - monoclonal paraprotein production **What is the pathophysiology?** free light chains of paraproteins precipitate in kidneys \> inflammation **What are the clinical features?** **_CRAB_** Calcium – HIGH Renal failure (acute or chronic) - ↑ urea ↑ Cr Why? Hypercalcaemia, paraprotein deposition Anaemia Bone – osteolytic bone lesions – pain, fracture (risk cord compression)
32
What are some nephrotoxic agents?
Examples: * Analgesics e.g. **NSAIDS** * Antibiotics e.g. **aminoglycosides – gentamicin, streptomycin** **•Contrast agents** * Anaesthetic agents * Chemotherapeutic agents **•ACE-I and ARBs** •Immunosuppressants e.g. ciclosporin, MTX
33
What can cause interstial nephritis?
* Drugs * Infections * Immune disorders e.g. SLE * Lymphoma * Tumor lysis syndrome following chemo
34
What are post renal causes of AKI?
**Luminal:** Stones, clots **Mural:** Malignancy (e.g. uteric, prostate, bladder), BPH, strictures **Extrinsic compression:** Retroperitoneal fibrosis
35
What is the management of AKI?
**General** * Assess volume status + Aim for euvolaemia * Stop nephrotoxic drugs (ACEi, ARBs, gentamicin, stop metformin if eGFR \<30) * Monitoring + Nutrition **Treat underlying cause** * _Pre-renal:_ Correct volume depletion with appropriate **fluids**, **antibiotics** (IF sepsis), **inotropes** (IF signs of shock) * **Post-renal**: **Catheterise** + imaging of renal tract **(CTKUB**) + urology + reversal * _Intrinsic renal_: **Refer** early to **nephrology** **Manage complications** * Hyperkalaemia: * Pulmonary oedema * Uraemia * Acidemia **Renal replacement therapy** – haemodialysis and haemofiltration if any complications are refractory to medical Mx
36
What are risk factors for CKD?
1. DM 2. HTN 3. CVS 4. Structural renal disease 5. multisystem disorders involving kidney 6. FHx 7. recurrent UTI 8. vesicoureteric reflux
37
How long does a loss of kidney need to be going on to be chronic?
3 months
38
What are the 2 most common causes of CKD? What are other causes of CKD?
1. Diabetes 2. Hypertension 3. Artherosclerosis 4. Chronic glorulonephritis 5. infective or obstructive uropathy 6. adult polycystic kidney disease (most common inherited cause)
39
What are signs and symptoms of CKD?
ASYMPTOMATIC unless really severe- usually incidental SEVERE symtoms: * Anorexia * Nausea and vomiting * Fatigue * Pruritus * Peripheral oedema * Muscle cramps * Pulmonary oedema * Sexual dysfunction is common Signs: rarely any signs! But if really bad can show signs complications: 1. Anaemia: conjunctival pallor 2. Uraemia: skin pigemnetation, excoriation 3. Bone disease: renal bone disease 4. peripheral vascular disease 5. hypertension 6. peripheral oedema
40
What are the consequences of CKD
1. Progressive failure of homeostatic function - Acidosis - Hyperkalaemia 2. Progressive failure of hormonal function - Anaemia - Renal Bone Disease - Osteomalacia 3. Cardiovascular disease - Vascular calcification - Uraemic cardiomyopathy 4. Uraemia and Death
41
What investigations do you do in CKD?
* Bloods: ↓Hb (normocytic anaemia); U&Es (↑urea/Cr), glucose (DM), eGFR, ↓Ca2+, ↑PO43−, ↑ALP (in renal osteodystrophy) ↑PTH if severe CKD * Urine: dipstick, MC&S, Protein:Cr ratio * Imaging: USS to check size/anatomy/cortico-medullarly differentiation and eliminate obstruction – in CKD kidneys are small (\<9cm) but may be enlarged in infiltrative disorders * CXR: Pericardial effusion or pulmonary oedema * Histology: consisted renal biopsy if rapidly progressing or unclear cause (C/I for small kidneys)
42
Management of CKD
1) Limiting progression/ complications * **BP:** target \<130/80 ( \<125/75 is diabetic) * Tight **glucose** control in DM * Decrease **CVS** risk ( stop smoking, lose weight etc) * Diet: multidisciplinary team: moderate protein, **restrict K+**, **avoid high phosphate foods**. * Reneal osteodystrophy: * •Calcichew - Ca supplement * Calcium acetate - phosphate binders * Cinacalcet (calcimimetic) – reduce PTH levels 2) Symptom control * •Anaemia: Human **EPO** might be required * Acidosis: Consider s**odium bicarbonate** supplements for patients with low serum bicarbonate. * Oedema: **loop diuretics, restriction of fluids** 3) Preparation for Renal Replacement Therapy * **Haemodialysis** – Vascular Access required * **Transplantation** – Gold standard treatment, Major surgery and long term immunosuppression.
43
44
What is the most common cause of a UTI? What other oragnism can cause it?
MOST COMMON: E coli **other causative organism:** * Staphylococcus saprophyticus * Proteus mirabilis * Enterococci Atypical organisms that can cause UTI (usually in **immunocompromised** individuals): * Klebsiella * Candida albicans * Pseudomonas aeruginosa
45
What are the different sub classifications of UTI's
* **_Lower UTI_** - affecting the urethra (urethritis), bladder (cystitis) or prostate * **_Upper UTI -_** affecting the renal pelvis (pyelonephritis)
46
What are the risk factors for UTI
* FEMALE * Sexual intercourse * Exposure to spermicide * Pregnancy * Menopause * Immunosuppression * Catheterisation * Urinary tract obstruction * Urinary tract malformation
47
How many GP consultations are for UTI?
1-3%
48
Sign and symptoms of a cystitis?
* Frequency * Urgency * Dysuria * Haematuria
49
What are signs and symptoms of Prostatitis?
* Suprapubic pain * Flu-like symptoms * Low backache * Few urinary symptoms
50
What are signs and symtoms of acute pyelonephritis?
* High fever * Rigors * Vomiting * Loin pain and tenderness * Oliguria (if AKI)
51
What are in general signs and symptoms of a UTI
Fever Abdominal or loin tenderness Foul-smelling urine Distended bladder (occasionally) Enlarged prostate (if prostatitis)
52
What are investigations and management of UTI?
**Investigations** * Urine **dipstick** (presence of nitrites) * MSU for urine **MCS** * Microscopy: **WBC** presence (pyuria) * **Culture**: provide colony forming unit * **Sensitivity** * **Bloods**: FBC, U&E, CRP * If complicated UTI - Renal USS/IV urography **Management** – _Follow local guidance_ * _Uncomplicated:_ **Cefalexin** 500mg PO BD *3*/7 OR **Nitrofurantoin** 50mg PO QDS 7/7 * If pregnant + BF: Cefalexin; Co-amoxiclav 62 * _Male:_ *7*/7 course of **Cefalexin** OR **ciprofloxacin** 500mg PO BD 14/7 (if suspicion of prostatits) * _Pyelonephritis/urosepsi_**s**: **Co-amoxiclav** 1.2mg IV ± amikaxin (CXH/HH) or gentamicin (SMH) first 1-2/7
53
What is important to rule out in patients with UTI?
other vaginal infections (chlamidya trachomatis) sterile pyuria Urogenital tract pathology
54
**Polycystic Kidney Disease** **Definition** **History** **Examination** **Investigation**
**Definition:** fluid filled cysts grow on the kidney, 10% of ESRF * Autosomal dominant inheritance, onset at 30-60 years * :1000 (85% of PKD1 Chr16, 15% PKD2 Chr4) **History**: clinically silent for many years! * Acute loin pain, stone formation, abdominal discomfort * Sx of renal failure * FHx of SAH (berry aneurysms) **Examination**: HTN, renal enalregment, abdominal pain ± haematuria **Investigations:** Haematuria, raised Hb, deranged U&E, abdominal USS, MRI angiography IF +ve 1st-degree SAH + ADPKD
55
What is PKD assosiated with (polycystic kidney disease)?
berry aneurysm in the circle of Willis
56
What is a renal carcinoma? What is the triad? What are other symptoms? What are the risk factors? What are the investigations?
**_What is a renal carcinoma?_** Neoplasm Arising from the renal parenchyma/cortex **_What is the triad?_** haematuria, loin pain, abdominal mass **_What are other symptoms?_** PUO, night sweats, rarely polycythemia if invades the left renal vein compresses left testicular vein = varicocele **_What are the risk factors?_** * Age * Smoking * Obesity * HTN * Dialysis (15%) * certain inherited syndromes (von Hippel-Lindau, tuberous sclerosis, familial papillary renal cell carcinoma) **_What are the investigations?_** * Increased **BP** (renin) * **Polycythaemia or IDA** (bleeding cysts) * **ALP** (bone mets) * **RBCs in urine,** * Cannon ball metastasis * filling defect ± calcification (CT/MRI i**ntravenous urogram IVU)**
57
**Renal artery stenosis** **Causes** **Clues** **Investigation**
**_Causes:_** Atherosclerosis (80%), fibromuscular dysplasia (10%, young F) **_Clues:_** * **↑ ↑ ↑ BP refractory to Tx** (1-5% of HTN) * **Worsening renal function after ACEi/ARB in bilateral RAS** * **Flash pulmonary oedema** (sudden onset, without LV impairment on echo) * Abdominal ± carotid or femoral bruits, weak leg pulses **Investigation:** * Ultrasound measurement of kidney size (affected size is smaller) * CT Angiogram or MR Angiography: risk of contrast nephrotoxicity * **Digital Subtraction Renal Angiography** = GOLD STANDARD (but invasive
58
Why do get hypertension in renal artery stenosis?
* Renal hypoperfusion (due to the stenosis) stimulates the renin-angiotensin system leading to increased angiotensin II and increased aldosterone * This leads to increased blood pressure * The high blood pressure leads to fibrosis, glomerulosclerosis and renal failure
59
**What drug should you not give someone with renal artery stenosis?** **Why not?**
**What drug should you not give someone with renal artery stenosis?** ACE INHIBITORS **Why not?** ACEi remove the efferent arterial tone - causing hypoperfusion and a sharp reduction in GFR
60
What are signs of someone with reanl artery stenosis?
* Hypertension * Signs of renal failure in advanced bilateral disease * Renal artery bruits
61
Someone comes in with 2/7 dysuria + frequency + offensive urine WHat investigation would you like to do?
MSU for MCS
62
someone comes in with Severe loin pain, vomiting & Haematuria on the dipstick What investigation would you like to do?
Non-contrast CT-KUB – most sensitive
63
Someone comes in with Recurrent UTI, FTT, baby FHx of vesico-ureteric reflux What investigation would you like to do?
USS of renal tract
64
Someone has just returned from India and has had weight loss, night sweats On the Urine dipstick there is blood and leukocytes The urine sample does not grow anything What investigations would you like to do
3 early morning urine samples for Microscopy, culture, ZN staining
65
Someone has had kidney Transplant (4/12 ago) and his renal function has worsened over 2/52 He also complains of pain around the area What investigation would you like to do?
Renal biopsy
66
What are the different types of stones compositions and what is the most commone
* _Calcium phosphate and calcium oxalat_e (**common**) – **radiopaque** * _Magnesium ammonium phosphate_ (struvite), **staghorn calculus** - associated with **urea-splitting bacteria (10-15%); klebsiella** * _Urate_ (uric acid)- associated with **gout, small bowel disease, tumour lysis syndrome** – **Radiolucent** (Mx: K+ citrate alkalise stone) * _Cysteine_ – **semi opaque**
67
How do you treat a ureteric stone?
68
Someone presents with Muddy brown cast + high creatinine High urine sodium, low urine osmolality Low urine:serum urea ratio Low urine:plasma osmolarity ratio What is your top differential for this?
Acute tubular necrosis
69
## Footnote Someone presents with Unwell after ACEi Bilateral renal bruits, Hx of IHD What is your top differential for this?
Pre-renal acute renal failure 2° renal artery stenosis
70
Someone presents with Esoinophilic cast, urine dip: protein+blood Old man, CAP, penicillin Tx, dysuria, back pain What is your top differential for this?
Acute interstitial nephritis
71
Someone presents with Bladder palpable up to umbilicus + unable to pass urine + man What is your top differential for this?
Post-renal AKI 2° to prostatic hypertrophy
72
Someone presents with D&V + high urea + creatinine + K+ Normocytic anaemia + fractionate RBC (film) Escherichia coli O157:H7 stool What is your top differential for this?
Haemolytic uraemic syndrome
73
Someone presents with HUS + Fever + neurological manifestations What is your top differential for this?
TTP
74
Someone presents with 24 years of rheumatoid + develop peripheral oedema Proteinuria 3+ urine – cause? What is your top differential for this?
Amyloidosis
75
Someone presents with Bone pain, lethargy, poor renal function Monoclonal band on serum electrophoresis Monoclonal globulin protein in urine What is your top differential for this?
Multiple myeloma
76
Someone presents with Crohn’s, poor renal function, proteinuria Stain +ve with congo red – renal Biopsy What is your top differential for this?
Amyloid A amyloidosis
77
Someone presents with T1DM albuminuria, previous dipstick normal What is your top differential for this?
Diabetic microalbuminuria
78
Someone presents with Collapse following stroke: High urea + creatinine, K+, High CK, urine dark red What is your top differential for this?
Rhabdomyolysis
79
Someone presents with 4M, facial swelling, 3+ proteinuria, low albumin What is your top differential for this?
Minimal change glomerulonephritis Electron microscopy: Fusion of podocytes
80
Someone presents with 25M, facial swelling, 3+ proteinuria, low albumin What is your top differential for this?
Membranous glomerulonephritis
81
Someone presents with +ve anti-GBM antibodies What is your top differential for this?
Goodpasture’s syndrome
82
Someone presents with 7M 2/7 after URTI hematuria, flank pain Biopsy: Proliferative glomerulonephritis with antibody deposition What is your top differential for this?
IgA nephropathy (Berger’s disease)
83
Someone presents with 15F, 2/52 post-tonsilitis, dark urine, puffy High titres of anti-streptolysin O antibody What is your top differential for this?
Post-strep glomerulonephritis

Meded Flashcards 2020 (36 decks)

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