CKD - amboss Flashcards

1
Q

define CKD

A

abnormality of kidney structure of function that persists > 3 months
common causes include diabetes, hypertension, and glomerulonephritis

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2
Q

pathos of diabetic nephropathy

A

hyperglycaemia causes varying degrees of damage to all types of kidney cells

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3
Q

pathos of hypertensive nephropathy

A

caused by protective autoregulatory vasoconstriction of preglomerular vessels
benign nephrosclerosis (sclerosis of afferent arterioles and small arteries
decreased perfusion
ischaaemic damage

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4
Q

pathos of glomerulonephritis

A

noninflammatory GN eg. membranous nephropathy, focal segmantal glomerulosclerosis
inflammatory GN eg. lupus nephritis, post streptococcal GN, rapid progressive GN, haemolutic uraemic syndrome

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5
Q

pathophys of CKD

A

reduced GFR causes decreased production of urine which leads to increase in extracellular fluid volume and total body volume overload
decrease in excretion of waste products eg. urea, drugs
decrease in excretion of phosphate causes hyperphosphataemia
decreased maintenance of acid base balance leads to metabolic acidosis
decrease in maintenance of electrolyte concentration causes electrolyte imabalances eg. Na retention

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6
Q

reduced endocrine activity in CKD

A

decrease in hydroxylation of calcifediol causes decreased production of calcitriol - decreased serum Ca
decreased in erythropoetin excretion causes decreased stimulation of erythropoiesis
reduced gluconeogenesis causes increased risk of hypoglycaemia

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7
Q

clinical features of CKD

A

patients are often asymptomatic until later stages due to the exceptional compensatory mechanisms of the kidneys
hypertension, heart failure, pulmonary oedema and peripheral oedema due to Na and H2O retention

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8
Q

define uraemia

A

accumulation of toxic substances due to decreased renal excretion. These toxic substances are mostly metabolites of proteins such as urea, creatinine, β2 microglobulin, and parathyroid hormone.

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9
Q

uremia symtpoms

A

constitutional: fatigue, weakness, headaches
GI symptoms: nausea and vomiting, loss of appetite, ammonia breath
derm: pruritis, skin colour changes, uremic frost
serositis: uremic pericarditis, pluritis
neuro: asterixis, uremic encephalopathy, peripheral neuropathy
haematologic: anaemia, leukocyte dysfunction, increased bleeding tendancy

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10
Q

uremic fetor

A

characteristic ammonia or urine like breath odour

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11
Q

uremic frost

A

uraemia leads to high levels of urea excreted in the sweat, the evaporation of which results in yellow white urea deposits on the skin

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12
Q

serositis

A

An inflammation of any serous surface such as the pericardium, pleura, or peritoneum. Usually associated with autoimmune diseases, such as systemic lupus erythematosus and rheumatoid arthritis.

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13
Q

uraemic pericarditis

A

complicaation of chronic kidney disease that causes fibrinous pericarditis
clinical features include chest pain worsened by inhalation
physical examination findings include friction rub on auscultation, ECG changes that would normlly be seen in non uremic pericarditis are not usually seen

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14
Q

signs of uraemic encephalopathy

A

seizures
somnolence
coma

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15
Q

criteria for chronic kidney disease

A

GFR < 60 for 3 months

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16
Q

define end stage renal disease

A

irreversible kidney dysfunction with GFR < 15 mL
manifesttions of uraemia requiring chronic renal transplant therapy with either dialysis or renal transplantation
likely death by cardiovascular disease

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17
Q

how do people with end stage renal disease usually die

A

Most likely due to associated complications (e.g., anemia of chronic kidney disease) and increased cardiovascular risk factors (e.g., hypertension)

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18
Q

CGA classification of chronic kidney disease

A

classified according to GFR and albuminuria
higher stages correlate with poorer prognosis

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19
Q

determining albuminuria category

A

Spot UACR: The ratio of urine albumin concentration to urine creatinine concentration. An ACR < 30 mg/g is considered normal to mildly increased; an ACR 30-300 mg/g for more than 3 months indicates likely chronic kidney disease. An ACR > 300 mg/g is severely increased.

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20
Q

other urine studies for CKD

A

Spot UPCR: The ratio of total protein to total creatinine in the urine. The UPCR obtained from a single urinary sample (i.e., spot urine) can be used to estimate 24-hour protein excretion (assuming creatinine is excreted at a constant rate). A spot UPCR value typically approximates the number of grams of protein excreted in the urine in a 24-hour period (e.g., a spot UPCR of 3.0 can be used to estimate proteinuria of ~ 3.5 g/day).
urine dipstick: may show hematuria or proteinuria
urine microscopy: may show abnormal urine sediment

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21
Q

US of kidneys and urinary tract

A

first line imaging technique for the assessment of kidney structure
conider obtaining for all patients to further support the diagnosis and help determine the etiology

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22
Q

findings on US suggesting chronic kidney disease

A

decrease in kidney length <10cm
decrease in parenchymal and/or cortical thickness
increase in cortical echogenicity
cysts
califications

23
Q

findings on US that suggests specific aetiologies

A

ureteral or renal pelvic dilation suggests obstructive nephropathy
bilaterally enlarged kidneys with multiple cysts suggest polycystic kidney disease

24
Q

CRAB criteria

A

The CRAB criteria indicate organ damage related to multiple myeloma: Calcium increased > 11 mg/dL, Renal insufficiency (creatinine clearance < 40 mL/min or serum creatinine > 2 mg/dL), Anemia (Hb < 10 g/dL), and Bone lesions.

25
suggestive features of renal artery stenosis
Treatment-resistant hypertension Abdominal bruit heard over the flank or epigastrium Evidence of other atherosclerotic diseases (e.g., CAD, PAD)
26
suggestive features of amyloidosis
History of a chronic inflammatory condition (e.g., IBD, RA) or chronic infectious disease (e.g., tuberculosis, osteomyelitis) History of plasma cell dyscrasia Evidence of other organ involvement (e.g., macroglossia, restrictive cardiomyopathy, hepatosplenomegaly, malabsorption)
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nutritional management
fluid intake - avoid dehydration protein restriction in patients with high CKD category sodium restriction pottisum intake adjustment phosphorous intake adjustment
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medication management
for renally cleared drugs - adjust dosing based on patients GFR avoid nephrotoxics contrast is highest risk in pateints with GFR < 30
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renal replacement therapy
non operative: haemodialysis or peritoneal dialysis operative: kidney transplatation
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dialysis indications
hemodynamic or metabolic complications that are refrectory to medical therapy eg volume overload or hypertension metabolic acidosis hyperkalaemia serositis other symptoms of uremia refrectory deterioration in nutritional status
31
ASCVD risk assessment
atherosclerotic cardiovascular disease screening for all patients with CKD diabetes mellitus screening screening for hypertension screening for lipid disorders cardiovascular risk
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blood pressure control
aim for systolic < 120 first line: RAAS inhibitors ie. ACE and ARBs consider combination therapy with calcium channel blocker or thiazide diuretic good blood pressure control is crucial to prevent ASCVD complications, reduce mortality and help delay disease progression in patients with CKD
33
lipid management
fasting lipid panel may show dyslipidaemia (high triglycerides are common) statin therapy for patients >50 or with comorbidities, or for treatment of ASCVD
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antiplatelet therapy
usualy indicated for management of ASCVD may be considered for primary prevention of ASCVD in high risk individuals
35
screening for CKD complications
FBC for normochromic, normocytic anaemia potassium for hyperkalaemia usually seen in advanced CKD PTH for secondary hyperparathyroidism hyperphosphataemia and hypocalcaemia typically seen with GFR < 30 Vit D monitoring shows decreased calcidiol and calcitriol coagulation screen blood gasses for metabolic acidosis
36
calcidiol
total body vit D stores
37
monitoring blood gasses
The kidneys are often no longer able to maintain acid-base balance when the GFR drops below 30 mL/min/1.73 m2. An accumulation of hydrogen ions leads to acidosis.
38
coagulation screening
normal PT, PTT and platelet count increased bleeding time due to uraemic platelet dysfunction
39
common acute complications of CKD
pulmonary oedema hyperkalaemia infection drug toxicity
40
pulmonary oedema
Due to an inability in patients with very low GFR to clear excess fluids
41
hyperkalaemia
May be triggered by excessive dietary potassium, nonadherence to diuretic therapy, or a new medication or medication interaction (e.g., ACE inhibitors, potassium-sparing diuretics)
42
infection as a complication
bacteraemia secondary to UTI or pneumonia IV catheter-related infection haemodialysis catheter related infection peritoneal dialysis-associated peritonitis
43
calciphylaxis
a rare but potentially life-threatening condition characterized by dermal and subcutaneous arteriolar calcifications that cause painful skin necrosis
44
riisk factors for calciphylaxis
Most commonly seen in patients with ESRD who are receiving dialysis Comorbidities: diabetes mellitus, obesity, CKD-mineral and bone disorder, warfarin therapy
45
clinical features of calciphylaxis
Intensely painful skin lesions, e.g.: livedo reticularis, purpura, plaques, nodules Necrotic skin ulcerations typically covered with black eschar Areas of firm, painful, subcutaneous tissue Secondary bacteremia and sepsis
46
diagnosis of calciphylaxis
A skin biopsy is required for definitive diagnosis but may provoke new lesions. Clinical diagnosis may be made in patients with ESRD with a typical presentation.
47
pathophys of anaemia of chronic kidney disease
decrease in synthesis of erythropoeitn decrease stimulation of RBC production normocytic, normochronic anaemia
48
management of anaemia in CKD
diagnostic studies forr iron deficiency B12 and folate deficiency erythropoeitn stimulating agenst avoid blood transfusions
49
CKD mineral and bone disorders
abnormalities in mineral and/or bone metabolism in CKD renal osteodystrophy refers specifically to issues with bone metabolism due to CKD
50
pathophysiology of CKD mineral and bone disorder
CKD causes hypocalcaemia via two mechanisms 1. decrease in renal excretion of phosphate, hyperphosphataemia, calcium phosphate precipitation 2. decrease in renal hydroxylation of vitamin D, decrease in calcitriol, decrease in intenstinaal Ca bsorption chronically decrease calcium level can caause secondary hyperparathyroidism, which can progress to tertiary hyperparaathyroidism
51
clinical features of CKD bone and mineral diseaase
fractures bone or periarticular pain muscular weakness and pain focal vascular calcification (atherosclerotic plaques) diffuse vascular calcification
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treatment of CKD bone and mineral disease
normlise phosphate, calcium and PTH levels dietary phosphate restriction phosphate binders treatment of hyperparathyroidism: supplimentation for vit D, calcimimetics, parathyroidectomy (last line)
53
secondary hyperprathyroidism
Excessive excretion of parathyroid hormone and hyperplasia of the parathyroid glands in response to low serum calcium levels. Causes include hypovitaminosis D and chronic kidney disease.
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