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Renal and Urology Flashcards

1
Q

Name some hormones that act on the kidney

A
  • Vasopressin from posterior pituitary - water resorption
  • Aldosterone from adrenal cortex - Na+ resorption
  • Natriuretic peptide - Na+ excretion
  • Parathyroid hormone - phosphate excretion, calcium resorption
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2
Q

Name some hormones produced by the kidneys

A
  • Renin (juxtaglomerular apparatus) - forms angiotensin II
    • Na+ retention and vasoconstriction
  • Vitamin D (metabolised by kidney into 1,25-DH cholecalciferol
    • Ca2+ and phosphate absorption from gut
  • Erythropoeitin
    • Red blood cell formation in bone marrow
  • Prostaglandin
    • Renal tone control
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3
Q

How is GFR regulated?

A
  • Myogenic - inc in BP stretches receptors in smooth muscle of vessels = vasoconstriction = inc resistance to flow = dec renal blood flow
  • Tubuloglomerular feedback mechanism - macula densa detects inc in NaCl (osmolarity) or inc flow rate
    • JGA signals via ATII or prostaglandins to vascoconstrict
    • Dec renal plasma flow = dec GFR = inc NaCl resorption = dec NaCl concentration at macula densa
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4
Q

Describe the RAAS system

A
  1. Dec ECF volume/dec BP detected by baroreceptors in arch of Aorta or carotid sinus
  2. Inc sympathetic activity to JGA = renin release
  3. Conversion of angiotensinogen to angiotensin I to angiotensin II via ACE
  4. ATII simulates glomerulosa to release aldosterone
    • Vasoconstricts
    • Increases Na+ resorption from PCT
    • Releases ADH - inc water retention - inc BP
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5
Q

How are UTIs classified?

A
  • Uncomplication
  • Complicated
    • Men
    • Abnormal renal tract/catheter/stent/
    • Impaired renal function
    • Immunosuppression/diabetes
    • Pregnancy
    • Elderly
  • Recurrent (further infections with new organism)
  • Relapse (further infections with same organism)
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6
Q

Name some risk factors for developing a UTI

A
  • Female
  • Sexual intercourse
  • Diabetes
  • Immunnosuppression
  • Pregnancy
  • Menopause
  • Urinary tract obstruction
  • Renal stones
  • Instrumentation
  • Diaphragm contraceptive
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7
Q

Name some common UTI organisms

A
  • E coli
  • Staph saprophyticus
  • Enterococcus faecalis
  • Klebsiella
  • Enterobacter
  • Pseudomonas aeruginosa
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8
Q

Describe the clinical features of UTI

A
  • Fever
  • Abdominal/loin/suprapubic tenderness
  • Frequency
  • Dysuria
  • Urgency
  • Haematuria
  • Polyuria
  • Cloudy urine
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9
Q

How is a UTI diagnosed?

A
  • Urine dip - proteinuria, leucocytes, nitrites, RBCs
  • MSU - M, C & S - if complicated, child or ill patient
    • Growth of >108 colony-forming units
  • Bloods if systemically unwell - FBC, U&E, CRP, blood cultures
  • Consider US/cystoscopy if child, men, recurrent, pyelonephritis
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10
Q

How is a UTI treated?

A
  • Advice - drink plenty, urinate often, post-intercourse voiding, wipe front to back
  • Antibiotics
    • Nitrofurantoin if GFR>45 100mg/BD
      • Uncomplicated 3 days
      • Complicated 7 days
    • Trimethoprim if allergic to nitro
    • Change to sensitive when MSU results come back
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11
Q

Name some causes of acute kidney injury

A
  • Pre-renal - reduced circulating volume
    • Hypovolaemia (haemorrhage, dehydration etc)
    • Cardiac failure
    • Liver failure
    • Shock
    • Renal artery stenosis/emboli
  • Intrinsic/renal
    • Acute tubular necrosis (ischaemia, drugs/toxins)
    • Drugs = gentamicin, NSAIDS, methotrexate, ACE-i, aminoglycosides
    • Toxins = myoglobin, sepsis, rhabdomyloysis
    • Glomerular disease (glomerular nephritis)
  • Post-renal = obstruction
    • Bladder outflow obstruction (BPH, strictures)
    • Tumour (prostate, bladder, gynae)
    • Stone (bilateral)
    • Retroperitoneal fibrosis
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12
Q

How is AKI investigated?

A
  • Low urine output ≈ <400ml/d
  • Urine dip - leucocytes, nitrites, blood, protein, glucose, ketones
  • Urine culture - M, C & S
  • Bloods - U&E (high urea, K+), high creatinine, osmolarity, FBC, LFT, clotting, CK, CRP
  • ABG (met acidosis)
  • Blood culture
  • If cause unclear consider - serum immunoglobulins, C3/C4, autoantibodies (ANA, ANCA, anti-ds DNA)
  • CXR - pulmonary oedema
  • ECG - hyperkalaemia?
  • Renal US
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13
Q

How can urine test results be used to distinguish pre-renal and renal causes of AKI?

A
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14
Q

How is AKI managed?

A
  • If bladder palpable - insert catheter
  • Stop nephrotoxic drugs
  • Treat underlying cause
    • Shock - fluids
    • Post-renal = catheter/nephrostomy
  • Dialysis if severe hyperkalaemia/metabolic acidosis, uraemic encephalopathy, pericarditis
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15
Q

Name some complications of AKI

A
  • Hyperkalaemia
  • Pulmonary oedema
  • Bleeding
    • Impaired haemostasis
  • Uraemic encephalopathy
  • Uraemic pericarditis
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16
Q

How is chronic kidney disease defined?

A

Progressive and irrervisble loss of renal function over years

  • 1 = GFR >90
  • 2 = GFR 60-89
  • 3 = GFR 30-59
  • 4 = GFR 15-29
  • End-stage = GFR < 15
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17
Q

Name some causes of CKD

A
  • Intrinsic
    • Glomerulonephritis/pyelonephritis
    • Polycystc kidneys
    • Bladder/urethral obstruction (BPH
    • Amyloidosis
  • Systemic
    • Diabetes
    • Hypertension
    • Gout
    • Heart failure
    • SLE
    • Renovascular
  • Drugs (gold, ciclosporin, analgesics)
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18
Q

Describe the clinical features of CKD

A
  • Yellow skin pigmentation
  • Brown nails
  • Purpura
  • Bruising
  • Hypertension
  • General - fatigue, weakness
  • Pulmonary oedema/dyspnoea
  • Cardiomegaly
  • Ankle swelling/peripheral oedema
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19
Q

How is CKD diagnosed?

A
  • Bloods - eGFR, normochromic, normocytic anaemia, U&E (high urea, creatinine) low calcium, high phosphate, high ALP, high PTH, high urate, CRP, glucose
  • Urine
    • Urinanalysis - blood, protein
    • Microscopy - WCC< granular casts, red cell casts
  • Imaging
    • Renal ultrasound - obstruction, PCKD
  • CXR - pulmonary oedema, cardiomegaly
  • Biopsy
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20
Q

How is CKD treated?

A
  • BP control (<130/80)
    • ACE-i with careful monitoring
  • Treat hyperlipidaemia with statins
    • Decrease risk of renovascular disease
  • Treat oedema with furosemide and metolazone
  • Treat anaemia
    • Consider erythropoeitin
  • Treat renal osteodystrophy (bone disease) with vit D analogues (alfacalcidol) and calcium supplements
  • Diet - protein restriction, Na+ and K+ restriction may be necessary
  • Dialysis
    • Peritoneal - insert Tenchkoff catheter
    • Haemo - AV fistula
  • Transplant
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21
Q

Name some complications of CKD

A
  • Fluid retention - oedema
  • Hypertension
  • CVS risk
  • Osteodystrophy (dec activated vit D = dec Ca2+ = PTH activation = bone resorption
  • Anaemia (dec erythropoeitin)
  • Electrolyte disturbance
  • Acidosis
  • Uraemia - anorexia, nausea, vomiting, pruritis
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22
Q

Name some common nephrotoxic drugs

A
  • NSAIDS
    • Incl. COX-2 inhibitors
  • Diuretics, ACE-i, ARB
  • Antibiotics - aminoglycosides, vancomycin
  • Immunosuppressants - ciclosporin, tacrolimus
  • Chemo - cisplatin
  • IV contrast
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23
Q

What is Acute Tubular Necrosis (ATN)?

A

A cause of AKI due to the death of tubular epithelial cells that form the renal tubules.

It is classified into toxic or ischaemic

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24
Q

What causes ATN?

A
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25
Q

Which patient groups are screened for CKD?

A
  • Hypertension
  • Diabetes
  • CCF
  • Atherosclerotic disease (coronary/cerebral/peripheral)
  • Multisystem diseases (SLE, myeloma)
  • Urological problems (outflow obstruction, renal stones)
  • Chronic nephrotoxin use
  • Unexplained haematuria or oedema
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26
Q

Describe the process of haemodialysis

A

Removal of toxins across a semi-permeable membrane

  • Concentration differences between dialysate (dialysis fluid containing physiological concentration of electrolytes) allow excess solutes to move down a contration gradient from blood to dialysate
  • Allows removal of waste products and excess water
  • Allows replacement of desirable molecules
  • 4 hours of treatment, 3 times a week in hospital or at home
  • Access via AV fistula or PTFE graft
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27
Q

How should AV fistulas be cared for?

A
  • No IV cannulae between elbow and wrist
  • Never use a tourniquet or BP cuff on fistula arm
  • Do not use fistula to take blood
  • Avoid using same site repetitively
  • Complications need immediate attention
    • Thrombosis
    • Infection
    • Aneurysm
    • Distal ischaemia
    • Extravasation
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28
Q

Name some complications of haemodialysis

A
  • Hypotension
  • Cramps
  • Infection
  • Nausea and vomiting
  • Headache
  • Haemolysis
  • Air emboli
  • Clotting of extracorporeal circuit
  • Malnutrition
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29
Q

Describe the process of peritoneal dialysis

A

Dialysate introduced into the peritoneal cavity via a Tenchkoff catheter. The peritoneal membrane acts as a semi-permeable membrane

  • 4-5 times a day
  • Loss of function after 5 years
  • At home by patient
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30
Q

What are the advantages of peritoneal dialysis?

A
  • Preservation of residual renal function
  • No need for vascular access
  • Mobility (holidays etc)
  • Patient engagement
  • Home-based therapy
  • Less expensive than haemo
  • Less risk of transmission of BBV
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31
Q

Name some contraindications of peritoneal dialysis

A
  • Patient/carer unable to train adequately in technique
  • Inguinal/umbilical/diaphragmatic hernias
  • Ileostomy or colostomy
  • Abdominal wall infections
    • Active diverticular disease
  • Peritoneal adhesions
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32
Q

Name some complications of peritoneal dialysis

A
  • Peritonitis
  • Catheter exit site infection
  • Drainage problems/occlusion
  • Peritoneal leaks
  • Pleural effusion
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33
Q

Name some contraindications for renal transplant

A
  • Active infection - CMV, zoster, HBV, hep B, TB, HIV
  • Cancer
  • Severe heart disease
  • Life expectancy < 5 years
  • Cirrhosis
  • Substance abuse
  • Morbid obesity
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34
Q

What types of graft are there in renal transplants?

A
  • Living Related Donor
    • HLA haplotype matching
    • Improved graft survival
  • Living unrelated Donation
  • Cadaveric
    • Donation after brain death (DBD)
    • Donation after cardiac death (DCD
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35
Q

Name some complications of renal transplants

A
  • Bleeding
  • Thrombosis
  • Infection
  • Oliguria
  • Rejection
    • Rising serum creatinine +/- fever, graft pain
    • Proteinuria
  • Ciclosporin nephrotoxicity
  • Infection
  • Malignancy
  • Hypertension
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36
Q

What investigated are needed before a transplant?

A
  • Immunological - blood group, HLA type, HLA antibody screen
  • Virology - HIV, Hep B/C, EBV, CMV, Varicella, toxoplasma, syphilis
  • Haematology - FBC, INR, Thrombophilia screen
  • CXR
  • ECG +/- additional cardiac assessments
  • Iliac doppler studies
  • US of native kidneys
37
Q

What immunosuppressive drugs are used in renal transplants?

A
  • Ciclosporin
  • +/- azathioprine/prednisolone

OR

  • Tacrolimus
  • Mycophenylate
38
Q

What is nephrotic syndrome?

A

The combination of proteinuria (>3.5/24hrs), hypoalbuminaemia (<30g/L) and oedema thought to be due to protein loss resulting in low albumin and low plasma oncotic plasma

39
Q

Name some causes of nephrotic syndrome

A

Primary:

  • Minimal change glomerulonephritis (common in young)
  • Focal segmental glomerulosclerosis
  • Membranous glomerulonephropathy (common in older)

Secondary:

  • SLE
  • Diabetes
  • Amyloidosis
40
Q

Name some clinical features of nephrotic syndrome

A
  • Facial swelling/peripheral oedema
  • Xanthelasma/xanthomata
  • Hypertension
  • Pleural effusion
  • Hepatomegaly
  • Ascites
  • Recurrent infections
41
Q

Name some complications of nephrotic syndrome

A
  • Susceptibility to infections
  • Thromboembolism
  • Hyperlipidaemia
  • Acute renal failure/AKI
42
Q

How is nephrotic syndrome investigated?

A
  • Urine dip - blood, proteins
  • Urine microscopy - RBCs, casts, M, C & S
  • Bloods - FBC, U&E, LFT, CRP, cholesterol, IGs, C3/C4, autoantibodies (ANA, ANCA)
  • Imaging
    • CXR
    • Renal US
  • Renal biopsy
43
Q

How is nephrotic syndrome treated?

A
  • Fluid and salt restriction
  • Avoid excess dietary protein
  • Control blood pressure
  • Control hyperlipidaemia
  • Diuretics (furosemide PO +/- metolazone (thiazide) or spironolactone
    • Reduce proteinuria
  • Treat underlying cause
    • Eg steroids in minimal change
    • Immunosuppressants in membranous
  • Heparin thromboprophylaxis if immobile
44
Q

What is nephritic syndrome?

A

Clinical syndrome associated with underlying glomerulonephritis:

  • Haematuria
  • Proteinuria
  • Hypertension
45
Q

Describe the clinical presentation of nephritic syndrome

A
  • Haematuria
    • Macro or microscopic +/- red cell casts
  • Proteinuria
  • Hypertension
  • Nephrotic syndrome signs
  • Renal failure
  • Oliguria
  • Signs of water and salt retention
46
Q

Name some causes of nephritic syndrome

A

Primary:

  • Glomerulonephritis
    • Minimal change
    • Rapidly progressive
  • IgA nephropathy/HSP

Secondary:

  • SLE (deposition of immune complexes)
  • Vasculitis
  • Diabetes
  • Post-streptococcal
  • Goodpasture’s
47
Q

What is Goodpastures syndrome?

A

Autoimmune attack of the type IV collagen in the basement membranes of the lungs and kidneys

48
Q

Describe IgA nephropathy

A
  • Primary glomerulonephritis cause of nephritic syndrome
  • Macroscopic haematuria
    • Precipitated by infection
  • Diagnosed via renal biopsy
  • No treatment
49
Q

How is nephritic syndrome diagnosed?

A
  • Bloods - FBC, U&E, LFT, CRP, Igs, complements, autoantibodies, anti-GBM, cultures, antistreptococcal antibody titres (ASOT) virology, creatinine
  • eGFR
  • Urine microscopy - RBC casts, M, C & S
  • Urine dip = blood, proteins
  • 24hr - protein/creatinine clearance
  • Imaging
    • CXR
    • Renal ultrasound
  • Renal biopsy
50
Q

How is nephritic syndrome treated?

A
  • Keep BP < 130/80
  • Salt and water restriction
  • Refer to nephrologist
  • Steroids / immunosuppressants
    • Need biopsy results to tailor to diagnosis
  • Dialysis
51
Q

What elements make up the glomerular filter?

A
  • Endothelial fenestrations
  • Glomerular basement membrane
  • Podocytes
52
Q

What is Alport’s syndrome?

A

Inherited genetic disease - defective type IV collagen genes result in thickened glomerular basement membrane with splitting of the lamina densa.

SIgns:

  • Progressive haematuria
  • Sensorineural deafness
  • Bulging of lens capsule
53
Q

What is respiratory acidosis? Name some causes

A

Lungs cannot remove enough CO2

  • Respiratory failure
    • COPD
    • Airway obstruction
    • Asthma
    • Mechanical chest injuries
    • Drugs - aneathesia, barbiturates
    • Injuries to respiratory centre in brain
54
Q

What is respiratory alkalosis? Name some causes

A

Too much CO2 is breathed off

  • Hyperventilation
    • Hypoxia detected by chemoreceptors
  • High altitude
  • Fever
  • Hysterical overbreathing
  • CNS causes
    • Stroke
    • Subarachnoid haemorrhage
    • Meningitis
55
Q

What is metabolic acidosis? Name some causes

A

The increased production of acids or excess loss of bicarbonate

  • High lactate (shock, infection, hypoxia)
    • Anaerobic respiration due to tissue hypoxia
  • DKA
  • Alcohol
  • Diarrhoea (loss of carbonate)
  • Renal disease (urate)
56
Q

What is metabolic alkalosis? Name some causes

A

Excess loss of acid

  • Vomiting/diarrhoea
  • Alkali ingestion
  • Diuretics (K+ depletion)
  • Decrease in ECF
    • Haemorrhage
    • Burns
57
Q

What are the parameters of pH, pCO2, HCO3-?

A

pH 7.35-7.45

pCO2 4.7-6.0kPa

HCO3- 22-28mmol/L

58
Q

Describe an approach to ABGs

A
  • pH: acidosis or alkalosis?
  • Is CO2 normal?
    • If raised - respiratory
    • If no change or opposite - compensated
  • Is HCO3- normal?
    • High - metabolic
    • No change or opposite - compensated
59
Q

What is the anion gap?

A
  • Estimates unmeasured anions

(Na+ and K+) - (Cl- and HCO3-)

  • Normal range 10-18mmol/L
  • Increased in metabolic acidosis due to increased production of fixed/organic acids (lactate, ketones, phosphate)
60
Q

Describe the appearance of respiratory acidosis, respiratory alkalosis, respiratory acidosis/alkalosis with metabolic compensation

A
61
Q

Describe the appearance of metabolic acidosis, metabolic alkalosis, metabolic acidosis/alkalosis with respiratory compensation

A
62
Q

What is base excess?

A

Marker of metabolic acidosis or alkalosis

  • High base excess (>2) indicated higher than normal HCO3-
    • Primary metabolic alkalosis
    • Compensated respiratory acidosis
  • Low base excess (<-2) indicates lower than normal HCO3-
    • Primary metabolic acidosis
    • Compensated respiratory alkalosis
63
Q

Name some signs and symptoms of hyponatraemia

A
  • Confusion
  • Seizures
  • Hypertension
  • Cardiac failure
  • Oedema
  • Nausea
  • Muscle weakness
64
Q

What causes hyponatraemia?

A
  • Loss through kidneys
    • Addisons
    • Renal failure
    • Excess diuretics (thiazides)
  • Loss elsewhere
    • Diarrhoea and vomiting
    • Burns
    • Small bowel obstruction
  • Water excess (oral/dextrose 5%)
  • SIADH
  • Organ failure - cardiac, liver, renal
  • Pseudohyponatraemia - serum volume increases from high lipids or proteins, Na+ falls but osmolarity is normal
    • Or taking blood from an arm with IV drip
65
Q

How is hyponatraemia diagnosed?

A
  • Is patient dehydrated?
  • Plasma Na+ < 135?
  • Is urinary Na+ > 20mmol/L?
  • Is patient oedematous?
  • Is urine osmolality > 500mmol/kg?
66
Q

How is hyponatraemia managed?

A
  • Correct underlying cause
  • Saline infusion
  • Furosemide
67
Q

Name some signs and symptoms of hypernatraemia?

A
  • Thirst
  • Confusion
  • Coma
  • Fits
  • Dehydration
    • Dry skin
    • Decreased skin turgor
    • Postural hypotension
    • Oliguria
68
Q

Name some causes of hypernatraemia

A

Plasma Na+ > 145

  • Fluid loss without replacement (diarrhoea, vomit, burns)
  • Incorrect IV fluid replacement (excess saline)
  • DIabetes insipidus
    • WIth large urine volume
  • Primary aldosteronism
    • If high BP, low K+ and alkalosis
69
Q

How is hypernatraemia managed?

A
  • Water orally if possible
  • Or dextrose 5% IV (4L/24hrs)
    • Guided by urine output
70
Q

Name some signs and symptoms of hyperkalaemia

A

Plasma K+ > 6.5

  • Cardiac arrhythmias
    • Palpitations
  • Sudden death
  • Muscle weakness
71
Q

What causes hyperkalaemia?

A
  • AKI/CKD
  • Excess K+ therapy
  • K+-sparing diuretics
  • Addisons (low aldosterone)
  • Low insulin
  • Rhabdomylosis
  • Massive blood transfusion
  • Metabolic acidosis (DKA)
  • Drugs - ACE-i, suxamethonium
72
Q

Describe the appearance of hyperkalaemia on an ECG

A
  • Tall tented T waves
  • Small P wave
  • Wide qrs complex
  • VF
73
Q

How is hyperkalaemia managed?

A
  • 10ml calcium gluconate IV over 2 mins
    • Provides cardioprotection
  • Insulin and glucose (20U soluble insulin and 50ml of glucose 50% IV)
    • Insulin moves K+ into cells
  • Nebulised salbutamol (2.5mg)
  • Polystyrene sulfonate resin + colonic irrigation
  • Dialysis
74
Q

Name some signs and symptoms of hypokalaemia

A
  • Muscle weakness
    • Paralysis of resp muscles
  • Hypotonia
  • Cardiac arrhythmia
  • Hyperpolarisation = decreased excitability = decreased APs
75
Q

Name some causes of hypokalaemia

A

K+ < 2.5

  • Diuretics
  • Cushings/steroids/ACTH
    • High insulin
  • Vomiting and diarrhoea
  • Conns syndrome
    • If high BP and alkalosis without diuretics
  • Pyloric stenosis
  • Alkalosis
76
Q

How is hypokalaemia managed?

A

If mild: >2.5

  • Oral K+ supplement (Sando K 2 tabs)

If severe: <2.5

  • IV potassium cautiously (no more than 20mmol)
    • Never as bolus
77
Q

How is calcium metabolism controlled?

A
  • Parathyroid hormone - inc PTH = inc plasma Ca2+ and dec PO43- due to reabsorption from bone and kidney
  • Vit D - inc Ca and Phos absorption from gut and kidney
    • Inhibits PTH
  • Calcitonin - dec Ca and Phos
  • Magnesium - Low Mag prevents PTH release
78
Q

What are the signs and symptoms of hypocalcaemia?

A
  • Tetany
  • Convulsions
  • Depression
  • Perioral parasthesia
  • Carpo-pedal spasm
    • Troussaeus sign (with BP cuff)
  • NM excitability
  • Cardiac arrhythmia
79
Q

What causes hypocalcaemia?

A
  • Thyroid/parathyroid surgery
  • If phosphate raised
    • Chronic renal failure
    • Hypoparathyroidism
    • Acute rhabdomyolysis
  • If phosphate normal or low
    • Osteomalacia (with high ALP)
    • Pancreatitis
  • Respiratory alkalosis
80
Q

How is hypocalcaemia treated?

A
  • Mild = calcium 5mmol/6hrs PO
  • Severe = 10ml of 10% calcium gluconate IV over 30min
  • Alfacalcidol
  • Correct underlying cause
81
Q

Name some signs and symptoms of hypercalcaemia

A
  • Bones = fractures, bone pain
  • Stones = renal stones/renal failure
  • Groans = abdo pain, constipation
  • Psychic moans = depression
  • Polyuria/polydipsia
  • Hypertension
82
Q

What are the causes of hypercalcaemia?

A
  • Malignancy - myeloma, bone mets, PTHrP
  • Primary hyperparathyroidism
  • Sarcoidosis
  • Acidosis
    • Increases free ca2+
    • Bone destruction
    • Drugs = thiazide
83
Q

How is hypercalcaemia diagnosed?

A
  • Albumin
  • Urea
  • Phosphate
  • ALP
  • PTH
84
Q

How is hypercalcaemia managed?

A
  • Fluids - rehydrate with saline
  • Treat hypokalaemia and hypomagnesaemia
  • Diuretics - furosemide 40mg/12hrs
    • AVOID thiazides
  • Bisphosphonates (pamidronate) - inhibit osteoclast activity
  • Treat underlying cause
    • Eg steroids for amyloidosis
85
Q

What is SIADH?

A

Hyponatraemia secondary to the dilutional effects of excessive water retention caused by increased ADH secretion

  • Decreased plasma osmolality
  • Increased urine osmolality (Na+ > 20)
  • Dehydrated
86
Q

Name some causes of SIADH

A
  • Small cell lung cancer
  • Pancreas/prostate malignancy
  • Stroke
  • Infections - pneumonia/TB
  • Drugs - sulfonylureas (glipizide) SSRIs
87
Q

How is SIADH managed?

A
  • Remove underlying cause
  • Fluid restriction
  • Slow correction of electrolyte imbalances with 0.9% saline and/or furosemide
    • Avoids central pontine myelinolysis
    • Demeclocycline = reduce responsiveness of collecting tubules to ADH
  • ADH (vasopressin) receptor antagonists
88
Q

Give examples of diuretics, where they work in the kidney and on what transporter

A
89
Q

What is the most common organism of an infected transplanted organ?

A

Cytomegalovirus

IPE (13 decks)

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