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Nephro 1 Flashcards

1
Q

What are the main functions of the kidney?

A

Filter and secrete waste/excess

Retain albumin and circulating cells

Reabsorb glucose, amino acids and bicarb

Control BP, fluid status and electrolyes

Activates 25-hydroxy Vit D –> 1,25 dihydroxy vitamin D (calcitriol)

Synthesis erythropoietin

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2
Q

What is the glomerular filtration rate?

A

Volume of fluid filtered from the glomeruli into Bowman’s space per unit time

120ml/min

7.2L/h

170L/day

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3
Q

What are characteristics of PCT?

A

Proximal Convoluted tubule

sugars, amino acids and bicarbonate get reabsorbed here

70% of Na+ absorbed and water follows

MOST vulnerable to damage

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4
Q

What is Fanconi syndrome?

A

not to be confused with FANCONI ANAEMIA

Proximal tubule insult (Wilson’s, tenofovir)

  • glycosuria
  • acidosis
  • phosphate wasting = rickets/osteomalacia
  • aminoaciduria
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5
Q

What are the functions of the loop of henle?

A

25% of Na+ absroved here and water follows

Thiazide diuretics work here

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6
Q

What are the functions of the distal convoluted tubule?

A

The juxtaglomerular apparatus

  • a solute sensing organ, if it detects HIGH SOLUTES - GFR is low = releases RENIN
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7
Q

What are the actions of Renin?

A
  1. It converts angiotensinogen to angiotensin-I
  2. ACE from lungs converts angiotensin 1 to 2
  3. This causes vasoconstriction and release of aldosterone
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8
Q

What are functions of the collecting duct?

A

salt handling, tightly regulated by aldosterone (increases reabsorption of Na+ in exchange for K+)

Secrete K+ and H+ into the urine

Water handling is also done here via Aquaporin 2 channels (these regulated by vasopressin)

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9
Q

How is potassium handled by the kidney?

A

K+ freely filtered and mostly reabsorbed in PROXIMAL TUBULE/LOOP OF HENLE

Governed by Na+ and Aldosterone

Insulin and catecholamines drive K+ uptake

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10
Q

What drugs cause hypokalaemia?

A

Loop diuretics and thiazide diuretics

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11
Q

What drugs cause hyperkalaemia?

A

spironolactone

amiloride

ACE-I

ARB

Trimethoprim

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12
Q

What is urinating regulated neurally?

A

S3,4,5 via parasympathetic - contract detrusor relax urethra

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13
Q

How is storage of urine regulated neurally?

A

T10, L1, L2 via sympathetic nervous system - RELAX bladder CONTRACT urethral sphincter

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14
Q

What are the 3 main narrowings where renal stones can lodge themselves?

A

Pelviureteric Junction

Pelvic Brim

Vesicoureteric Junction

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15
Q

What are most renal stones made of?

A

Calcium oxalate and Phosphate

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16
Q

What are some risk factors for renal stones?

A

Anatomical abnormalities

Chemical composition of urine that favours stone crystallisation

Dehydration

Infection

Increased Ca, Oxalate, Urate

Primary renal disease

Drugs - diuretics, antacids, acetazolamide, corticosteroids

Chocolate, rhubarb

Gout

Fam Hx

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17
Q

How would renal stones/renal colic present?

A

Asymp

Renal Colic - rapid onset, loin to groin, comes and goes in waves, nausea and vomiting, worse with fluid loading

Dysuria, strangury (burning when peeing), frequency

Recurrent UTI’s

haematuria

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18
Q

How would you investigate renal colic?

A

Urinalysis - maybe normal, exclude other causes

FBC - WBC to rule out infection

Serum electrolytes, urea and creatinine - hypercalcaemia, hyperuricaemia

Urine pregnancy test - ectopic

non-contrast CT

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19
Q

How would you treat renal stones/colic?

A

Conservative - overhydration, low Ca, dietary intake, low sodium, reduced BMI, reduced animal proteins

Morphine

Ondansetron

Abx - trimethoprim/nitro

Surgical decompression

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20
Q

What are some pre-renal causes of AKI?

A

40-70%

Renal hypoperfusion (hypovolaemia or sepsis)

Hypotension without hypovolaemia (cirrhosis or septic shock)

Low cardiogenic output (cardiac failure/cardiogenic shock)

Renal hypoperfusion (NSAIDs, ACE-inhibitors)

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21
Q

What are some intrinsic renal causes of AKI?

A

10-50%

Renal parenchyma damage

Acute tubular necrosis (NSAIDs, radiological contrast, uric acid crystals, myeloma)

Vascular

  • renal artery/vein thrombosis
  • cholesterol
  • vasculitis
  • haemolytic uraemic syndrome
  • malignant hypertension

Glomerular- glomerulonephritis, SLE, drugs, infection

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22
Q

What are some post-renal causes of AKI?

A

UTI

Luminal - stones, clots

Mural - malignancy, BPH, strictures

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23
Q

What are risk factors for AKI?

A

> 75

HF

Peripheral vascular disease

Sepsis

Poor fluid intake

CKD

Hypovolaemia

Diabetes

Prostate cancer

Nephrotoxic drugs

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24
Q

How does AKI present?

A

Oliguria

Arrythmias - hyperkalaemia

Uraemia - fatigue, weakness, anorexia, N&V, confusion, seizures and coma

Anaemia and pulmonary oedema - breathlessness

Pericarditis

Impaired platelet function

Postural hypotension

Thirst

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25
How would you investigate AKI?
basic metabolic profile - elevated creatinine, high potassium serum urea to creatinine ratio = 20:1 supports pre-renal Urinalysis urine culture FBC - anaemia, leucocytosis, thrombocytopenia VBG - met acidosis fluid challenge - renal function will improve in pre-renal azotaemia bladder catheterisation
26
What is a staging system for AKI?
KDIGO based on serum creatinine and urine output
27
How would you treat AKI?
Volume expansion and/or red blood cell transfusion - normal saline Vasopressor - dopamine/adrenaline Diuretic - furosemide Renal replacement therapy - haemodialysis for 4-6 hours Hyperkalaemia - calcium gluconate + insulin and glucose to drive K+ into cells Acidosis - sodium bicarb
28
What is acute nephritic syndrome characterised by?
also known as acute glomerulonephritis Haematuria - visible or non-visible Proteinuria (usually <2g in 24 hrs) Hypertension Oedema (periorbital, leg or sacral)
29
What are some causes/RFs of acute nephritic syndrome?
Often immune response to infection of another disease IgA nephropathy (most common primary cause) - bacterial (MRSA, typhoid, secondary syphilis) - Hep B, C - Schistomiasis - Malaria - Post-strep infection 0 classically 2 weeks after tonsilittis - Infective endocarditis - SLE - ANCA assoc. vasculitis - Goodpastures
30
What is IgA nephropathy?
Commonest cause of nephritic syndrome Haematuria, IgA deposition in mesangium of kidney Assoc. with tonsillitis and results in haematuria
31
What is goodpasture's?
co-existence of acute glomerulonephritis and pulmonary alveolar haemorrhage, circulating antibodies directed against an intrinsic antigen to the basement membrane of both kidney and lung
32
How would you investigate acute glomerulonephritis?
Urinalysis - haematuria, proteinuria, dysmorphic RBCs, leukocytes and RBC casts Met profile - creatinine, hypoalbunaemia LFTs GFR FBC - normocytic normochromic anaemia Lipid profile USS of kidneys
33
How would you manage acute glomerulonephritis?
Phenoxymethylpenicillin Furosemide Prednisolone IF SEVERE - plasmapheresis + corticosteroid + cyclophosphamide
34
What is the classical triad of nephrotic syndrome? What else might you see?
Proteinuria - frothy urine Hypoalbunaemia Oedema - pitting oedema of ankle, genital , abdo wall and sometimes periorbital *severe hyperlipidaemia - liver goes into overdrive due to albumin loss and other protein loss which increases risk of blood clots and raised cholesterol
35
What are the causes/RFs of nephrotic syndrome?
Structural and functional abnorm of podocytes Minimal change disease - commonest cause Membranous nephropathy - penicillamine, gold, NSAIDs, SLE, thyroiditis, Hep B, C, schistomiasis, neoplasia Focal segmental glomerulosclerosis Diabetes Amyloid Infections SLE, RA
36
How would you investigate nephrotic syndrome?
Renal biopsy - establish cause urine dip - very high protein CXR or USS for pleural effusion or ascites Albumin low Creatinine, eGFR, lipids and glucose SLE - ANA, dsDNA, C3, C4 Hep B antigen, Hep C antibody
37
How would you manage nephrotic syndrome?
Oedema - furosemide, fluid and salt restriction Proteinuria - ACEi, ARB Complications - warfarin, simvastatin
38
What is minimal change disease? What are causes/RFs?
Commonest cause of nephrotic syndrome in children - boys under age of 5 characterised by minimal histological changes in the kidney Idiopathic Atopy - in 30% Drugs - NSAIDs, lithium, Abx, Bisphos, Sulfasalazine Hep C, HIV, TB
39
How would you treat minimal change disease?
Corticosteroid - prednisolone Fluid restriction and low -salt Albumin and furosemide
40
What is CKD?
longstanding, usually progressive, impairment in renal function for more than 3 months GFR <60mL/min/1.73m2 for more than 3 months with/without evidence of kidney damage
41
Causes/RFs for CKD?
``` Diabetes HTN Atherosclerotic renal vascular disease PKD Tuberous sclerosis IgA nephropathy SLE Amyloidosis Smell and medium-sized vessel vasculitis ``` Fam Hx CKD
42
Presentation of CKD?
Early stages could be asymptomatic ``` Malaise Anorexia Weight loss Insomnia Nocturia Polyuria itching N&V and diarrhoea Amenorrhoea and ED in men ```
43
What are some complications assoc. with CKD?
anaemia - normochromic normocytic anaemia bone disease - bone pain, osteo-malacia, hyperparathyroidism neurological - autonomic dysfunction (postural hypotension, disturbed GI motility), peripheral paraesthesiae CVS - MI, cardiac failure, sudden cardiac death and stroke Skin disease - pruritus, brown discolouration of nails
44
How would you investigate CKD?
ECG - high potassium Urinalysis - haematuria, proteinuria, MC&S, albumin to creatinine ratio Biochem - urea, electrolytes, bicarb and creatine, low eGFR, raised ALK phos Immunology - screen for SLE, scleroderma,and goodpastures Hep B, C, HIV USS - renal size CT - detect stones
45
How is CKD staged?
According to GFR Stage 1 = >90 normal Stage 2 = 60-89 Stage 3A = 45-59 Stage 3B = 30-44 Stage 4 = 15-29 Stage 5 = <15
46
How would you treat CKD?
Stage 1-2 without uraemia ACE/ARB Statin Atenolol CCB - verapamil Stage 3-4 without uraemia ACE/ARB Statin + ezetimibe Atenolol Educate about renal replacement therapy Stage 5 or with uraemia Dialysis Kidney transplant Sevelamer Calcimimetic
47
What are the types of renal cystic disease?
AD PKD | AR PKD
48
What is the genetics behind PKD?
AD Homozygous - die in womb mutations in PKD1 (85%) gene in chromosome 16 mutations in PKD2 (15%) gene on chromosome 4
49
How does ADPKD present?
clinically silent for years Symptoms normally 20s onwards ``` Loin pain haematuria loin or abdominal discomfort nocturia renal colic hypertension renal stones progressive renal failure ```
50
What are extra-renal presentation of ADPKD?
subarachnoid haemorrhage - berry aneurysm rupture Polycystic liver disease (70%) Pancreatitis Mitral valve prolapse Ovarian cysts Diverticular disease
51
How would you investigate ADPKD?
Renal USS/CT <30 y/o - atleast 2 unilateral or bilateral cysts 30-59 y/o - 2 cysts in each kidney >60 y/o - 4 cysts in each kidney urinalysis serum electrolytes, urea, creatinine fasting lipid profile ECG CT head - check for ruptured intracranial aneurysm
52
Treatment of ADPKD?
nothing can slow progression BP - control ACE-I Laparoscopic removal of cysts Serial monitoring of creatinine to track disease progression
53
What mutation for ARPKD?
PKHD1 mutation on long arm (q) of chromosome 6 Fam hx
54
What is acute interstitial nephritis? causes?
25% of drug-induced acute kidney injury. ``` penicillin rifampicin NSAIDs allopurinol furosemide ``` SLE sarcoidosis
55
How would you investigate acute interstitial nephritis?
urea and creatinine Urine Hansel's or Wright's eosinophil stain - eosinophiluria urinalysis - microhaematuria, sterile pyuria, proteinuria trial of discontinuing offending medication ANCA, ANA negative
56
How does acute interstitial nephritis present?
fever rash oedema plus AKI and hypertension
57
Differences between IgA nephropathy and post-streptococcal glomerulonephritis?
Recent URTI Haematuria IgA after 1-2 days and PSG 1-2 weeks after URTI PSG - proteinuria
58
For renal transplant, how are donors matched?
based on human leukocyte antigen
59
What is a typical renal transplant scar? What medications can be given for immunosuppression?
Hockey stick incision - hockey stick scar Tacrolimus Mycophenolate Prednisolone
60
What is acute tubular necrosis?
damage and death of epithelial cells of the renal tubules - most common cause of AKI takes 7-21 days to recover
61
What causes acute tubular necrosis? What would be typical on investigations?
Shock Sepsis Dehydration Radiology dye NSAIDs Heroin Muddy brown casts on urinalysis is pathognomonic!! Aso renal tubular epithelial cells in urine
62
What are the different types of renal tubular acidosis?
Type 1 - distal tubule pathology (unable to excrete hydrogen ions) Type 2 - proximal tubule pathology (unable to reabsorb bicarb from urine) Fanconis Type 3 - combination of type 1 and type 2 Type 4 - reduced aldosterone (adrenal insufficiency, ACE, spironolactone, SLE) - treat with fludrocortisone, sodium bicarb and treat hyperkalaemia
63
Presentation of Rhabdo? Investigations?
``` Muscle aches and pain Oedema Fatigue Confusion Red-brown urine ``` CK - rises until 21 hrs and then remains elevated for 1-3 days Myoglobinurea - red-brown colour in urine U&Es ECG - hyperkalaemia
64
Treatment of Rhabdo?
IV fluids consider sodium bicarb consider IV mannitol - to increase gfr and reduce oedema Treat hyperkalaemia

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