bobrek Flashcards
causes of Unintentional weight loss in elderly and next step maangment
ckd, copd, hf
nutritional supplement
All diabetic patients with a urinary ACR of 3 mg/mmol or more should be started on —–
ACE inhibitor or angiotensin-II receptor antagonist
Diabetic nephropathy: management
dietary protein restriction
tight glycaemic control
BP control: aim for < 130/80 mmHg
ACE inhibitor or angiotensin-II receptor antagonist
should be start if urinary ACR of 3 mg/mmol or more
dual therapy with ACE inhibitors and angiotensin-II receptor antagonist should not be started
control dyslipidaemia e.g. Statins
screening of diabetic neuropathy
all patients should be screened annually using urinary albumin:creatinine ratio (ACR)
should be an early morning specimen
ACR > 2.5 = microalbuminuria
drugs causing hyperthyroidims
amiodarone, lithium, chemo drugs
Wilms’ nephroblastoma features
Features
abdominal mass (most common presenting feature)
flank pain
painless haematuria
other features: anorexia, fever
unilateral in 95% of cases
metastases are found in 20% of patients (most commonly lung)
painless visible hematuria-elderly-dx
transitional cell carcinoma of bladder
The maximum recommended rate of potassium infusion via a peripheral line is
10 mmol/hour, whereas rates above 20 mmol/hour require cardiac monitoring
maintenance fluid requirements
—– ml/kg/day of water and
approximately
—-mmol/kg/day of potassium, sodium and chloride and
approximately ——g/day of glucose to limit starvation ketosis
25-30 ml/kg/day of water and
approximately 1 mmol/kg/day of potassium, sodium and chloride and
approximately 50-100 g/day of glucose to limit starvation ketosis
0.9% saline
if large volumes are used there is an increased risk of ——–
0.9% saline
if large volumes are used there is an increased risk of hyperchloraemic metabolic acidosis
aki prerenal
hypovolaemia secondary to diarrhoea/vomiting
renal artery stenosis
aki intrinsic
glomerulonephritis
acute tubular necrosis (ATN)
acute interstitial nephritis (AIN), respectively
rhabdomyolysis
tumour lysis syndrome
postrenal aki
kidney stone in ureter or bladder
benign prostatic hyperplasia
external compression of the ureter
aki symptoms
reduced urine output
pulmonary and peripheral oedema
arrhythmias (secondary to changes in potassium and acid-base balance)
features of uraemia (for example, pericarditis or encephalopathy)
aki detection
U&Es=sodium
potassium
urea
creatinine
Urinalysis
all patients with suspected AKI should have urinalysis
Imaging
if patients have no identifiable cause for the deterioration or are at risk of urinary tract obstruction they should have a renal ultrasound within 24 hours of assessment.
management aki
-Stabilisation of the cardiac membrane
-Short-term shift in potassium from extracellular to intracellular fluid compartment
-Removal of potassium from the body
Stabilisation of the cardiac membrane
* Intravenous calcium gluconate
Short-term shift in potassium from extracellular to intracellular fluid compartment
* Combined insulin/dextrose infusion
* Nebulised salbutamol
Removal of potassium from the body
* Calcium resonium (orally or enema)
* Loop diuretics
* Dialysis
Causes of transient or spurious non-visible haematuria
urinary tract infection
menstruation
vigorous exercise (this normally settles after around 3 days)
sexual intercourse
Causes of persistent non-visible haematuria
cancer (bladder, renal, prostate)
stones
benign prostatic hyperplasia
prostatitis
urethritis e.g. Chlamydia
renal causes: IgA nephropathy, thin basement membrane disease
Spurious causes - red/orange urine, where blood is not present on dipstick
foods
drugs
foods: beetroot, rhubarb
drugs: rifampicin, doxorubicin
hyperkalemia management
-iv gluconate
-insulin/dextrose infusion
-nebulised salbutamol
-calcium resonium
-loop diuretics
-dialysis
-stop ace-i
Primary hyperaldosteronism causes —–, by retaining more —- and excreting more ——. As a consequence, more —— will be expelled, causing —–.
Primary hyperaldosteronism causes metabolic alkalosis, by retaining more sodium and excreting more potassium. As a consequence, more hydrogen ions will be expelled, causing alkalosis.
The anion gap is calculated by:
A normal anion gap is
(sodium + potassium) - (bicarbonate + chloride)
A normal anion gap is 8-14 mmol/L
Causes of a normal anion gap or hyperchloraemic metabolic acidosis
gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula
renal tubular acidosis
drugs: e.g. acetazolamide
ammonium chloride injection
Addison’s disease
Causes of a raised anion gap metabolic acidosis
lactate: shock, hypoxia
ketones: diabetic ketoacidosis, alcohol
urate: renal failure
acid poisoning: salicylates, methanol
5-oxoproline: chronic paracetamol use
Patients with chronic kidney disease should be started on ==== if they have an ACR > 30 mg/mmol
Patients with chronic kidney disease should be started on an ACE inhibitor if they have an ACR > 30 mg/mmol
ckd-diabetic nephropathy –clinical sign
proteinuria
ACR-albumin/creatinine ratio for quantification of proteinuria
The most likely renal outcome for the 13-year-old girl with Henoch-Schonlein purpura (HSP) and mild renal impairment is ====. HSP, also known as IgA vasculitis, is a small-vessel vasculitis that predominantly affects children. While it can cause kidney involvement in the form of IgA nephropathy, most cases of HSP with renal involvement have a good prognosis and recover fully without any long-term complications.
features:
treatment:
The most likely renal outcome for the 13-year-old girl with Henoch-Schonlein purpura (HSP) and mild renal impairment is full renal recovery.
=Features
palpable purpuric rash (with localized oedema) over buttocks and extensor surfaces of arms and legs
abdominal pain
polyarthritis
features of IgA nephropathy may occur e.g. haematuria, renal failure
=Treatment
analgesia for arthralgia
treatment of nephropathy is generally supportive. There is inconsistent evidence for the use of steroids and immunosuppressants
=bp monitor and urinalysis to detect renal involvement
Normocytic anaemia==, thrombocytopaenia and AKI following diarrhoeal illness - consider ==
investigations:
managements:
Normocytic anaemia-microangiopathic hemolytic anemia, thrombocytopaenia and AKI following diarrhoeal illness - consider HUS
e.coli-0157:h7
Investigations
full blood count
anaemia: microangiopathic hemolytic anaemia characterised by a haemoglobin level less than 8 g/dL with a negative Coomb’s test
thrombocytopenia
fragmented blood film: schistocytes and helmet cells
U&E: acute kidney injury
stool culture
looking for evidence of STEC infection
PCR for Shiga toxins
Management
treatment is supportive e.g. Fluids, blood transfusion and dialysis if required
there is no role for antibiotics, despite the preceding diarrhoeal illness in many patients
the indications for plasma exchange in HUS are complicated
as a general rule plasma exchange is reserved for severe cases of HUS not associated with diarrhoea
eculizumab (a C5 inhibitor monoclonal antibody) has evidence of greater efficiency than plasma exchange alone in the treatment of adult atypical HUS
Focal segmental glomerulosclerosis (FSGS) is a cause of nephrotic syndrome and chronic kidney disease. It generally presents in young adults.
Causes:
idiopathic
secondary to other renal pathology e.g. IgA nephropathy, reflux nephropathy
HIV
heroin
Alport’s syndrome
sickle-cell
Membranous glomerulonephritis histology:
Membranous glomerulonephritis histology:
basement membrane thickening on light microscopy
subepithelial spikes on sliver stain
positive immunohistochemistry for PLA2
Membranous glomerulonephritis causes
idiopathic: due to anti-phospholipase A2 antibodies-dvtye neden oluyo
infections: hepatitis B, malaria, syphilis
malignancy (in 5-20%): prostate, lung, lymphoma, leukaemia
drugs: gold, penicillamine, NSAIDs
autoimmune diseases: systemic lupus erythematosus (class V disease), thyroiditis, rheumatoid
==== is the first indicator of diabetic nephropathy. Management includes blood pressure and proteinuria control with an ==== or ==
Microalbuminuria is the first indicator of diabetic nephropathy. Management includes blood pressure and proteinuria control with an ACE-inhibitor or ARB
lactic acidosis type A: ====
lactic acidosis type B: ===
lactic acidosis type A: sepsis, shock, hypoxia, burns
lactic acidosis type B: metformin
Causes of normal anion gap metabolic acidosis
Diarrhea
Fistulae (eg, pancreatic, ileocutaneous, etc.)
Carbonic anhydrase inhibitors
Renal tubular acidosis
Ureteral diversion (eg, ileal loop)
Iatrogenic
Non-anion gap metabolic acidosis and hyperkalemia that occur out of proportion to the renal dysfunction indicate a ——–.
Non-anion gap metabolic acidosis and hyperkalemia that occur out of proportion to the renal dysfunction indicate a renal tubular disorder.
rta 4
Impaired function of the cortical collecting tubule due to aldosterone deficiency or resistance will cause retention of H+ and K+ and is termed hyperkalemic RTA Hyperkalemic RTA is commonly seen in elderly patients who have poorly controlled diabetes with damage to the juxtaglomerular apparatus, which causes a state of hyporeninemic hypoaldosteronism.
loop diuretics cause
hypokalemia, metabolic alkalosis
laxative abuse causes
hypokalemic metabolic alkalosis
primary hyperaldesteronism causes
hypokalemia metabolic alkalosis
renal artery stenosis causes
secondary hyperaldesteronism, hypokalemia, metabolic alkalosis, hypertension
vomiting causes
hypochloremic metabolic alkalosis-due to loss of gastric hcl, hypokalemia can happen due to increased aldosterone secretion due to volume depletion
sarcoidosis manifestations
pulm-
cutaneous-
opht-
neuro=
cvs=
gastro=
systemic=
Pulmonary
Hilar lymphadenopathy*
Interstitial infiltrates
Cutaneous
Papules, nodules & plaques
Erythema nodosum*
Ophthalmologic
Anterior & posterior uveitis
Keratoconjunctivitis sicca
Neurologic
Facial nerve palsy
Central diabetes insipidus
Hypogonadotropic hypogonadism
Cardiovascular
AV block
Dilated or restrictive cardiomyopathy
Gastrointestinal
Hepatosplenomegaly
Asymptomatic LFT abnormalities
Other
Hypercalcemia
Peripheral lymphadenopathy
Parotid gland swelling
Polyarthritis*
Constitutional symptoms (fever,* malaise)
*Manifestations of Löfgren syndrome.
AV = atrioventricular; LFT = liver function test.
causes of hypercalcemia
-hyperpth
-solid malignancies
-osteolytic malignancies
-granulomatous disease, lymphoma
calcium metabolism
-pth
-vit d
-calcitonin
-pth=↑ Bone resorption
↑ Renal reabsorption of calcium & ↓ reabsorption of phosphate
↑ Conversion of 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D
-vit d=↑ Intestinal absorption of calcium & phosphate
↑ Renal reabsorption of calcium & phosphate
↓ Parathyroid hormone secretion
↑ Mineralization of bone
-calcitonin=↓ Bone resorption
↓ Renal calcium reabsorption
sarcoidosis pathophys
-extrarenal calcitriol conversion in macrophages of lungs and lymph nodes
-pth independent
-increased calcitriol=intestinal calcium absorption increases=hypercalcemia
-pth decreases due to negative feedback by hypercalcemia and increased calcitrio
-Renal calcium reabsorption decreases due to low PTH; because serum calcium is high, renal calcium excretion increases=hypercalciuria
Refeeding syndrome occurs in the setting of ==, typically due to ===(eg, alcohol use disorder, anorexia). Patients with alcohol use disorders are at particularly elevated risk due to alcohol-induced ===(reduces intestinal == absorption) and == (==-based antacids bind intestinal ===).
Refeeding syndrome occurs in the setting of hypophosphatemia, typically due to chronic malnutrition (eg, alcohol use disorder, anorexia). Patients with alcohol use disorders are at particularly elevated risk due to alcohol-induced chronic diarrhea (reduces intestinal phosphate absorption) and gastritis (calcium-based antacids bind intestinal phosphorus).
Glomerulonephritis is typically accompanied by evidence of
glomerular damage on urinalysis (eg, dysmorphic red blood cells, red blood cell casts).
Chronic pyelonephritis may cause
Chronic interstitial nephritis with WBCs and WBC casts. However, this typically occurs as a sequela of recurrent acute pyelonephritis with prior symptoms of dysuria, fever, and recurrent flank pain (absent in this patient).
aki=
oliguria/anuria
signs of uremia=anorexia/nausea/asterixis/pericarditis/platelet dysfunction, fatigue, confusion
how to manage?
-confirm aki diagnosis and stage
-labs-cbc/bmp/calcium, phosphate, magnesium, and ABG or VBG
-Urine studies: urinalysis, urine microscopy, urine chemistry (sodium, urea, osmolality, creatinine)
- Consider urgent ultrasound and/or foley catheter placement (if urinary tract obstruction is suspected).
- Consider early nephrology consult.
-Optimize volume status.
-Identify and treat any metabolic complications (e.g., acidosis, hyperkalemia).
-Identify and treat the underlying cause.
-Hold nephrotoxic medications and renally-dose other medications.
-Strict input/output monitoring
-Provide additional supportive care (e.g., nutritional support, VTE prophylaxis)
prerenal aki causes
- decreased renal blood flow (RBF) and GFR.
- decreased RBF may be 2ndary to hypovolaemia per se, decreased effective RBF (decreased cardiac
output, vasodilatation in sepsis), or intrarenal vasomotor changes (e.g.
NSAIDs and ACE-I). - Potentially reversed by restoration of RBF.
- Kidneys remain structurally normal.
commonest cause of intrinsic aki
atn
Dialysis disequilibrium syndrome
risk factors
management
complications
the development of acute cerebral edema secondary to the rapid extraction of osmotically active substances (e.g., urea, NaCl) from the blood
-Risk factors [18]
First dialysis sessions
Extremely elevated BUN
Metabolic acidosis
Preexisting neurological abnormalities
Hyperglycemia or hypernatremia
-Management: Monitor patients for symptoms of cerebral edema and initiate management of raised ICP if present.
-Other complications [2][7]
Acquired cystic kidney disease [19]
Cramps
Electrolyte abnormalities, e.g., hypophosphatemia
Dialysis-related amyloidosis, which can cause carpal tunnel syndrome [20][21]
Allergic reaction to the equipment or dialysate [3]
the leading cause of death in patients on dialysis and kidney transplant recipients
cardiovascular disease
A unique phenotype of kidney injury in patients with cirrhosis and ascites in the absence of hypovolemia or other kidney pathology
hepatorenal syndrome
