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Internal Med 2023 > CKD - amboss > Flashcards

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
Q

suggestive features of renal artery stenosis

A

Treatment-resistant hypertension
Abdominal bruit heard over the flank or epigastrium
Evidence of other atherosclerotic diseases (e.g., CAD, PAD)

26
Q

suggestive features of amyloidosis

A

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)

27
Q

nutritional management

A

fluid intake - avoid dehydration
protein restriction in patients with high CKD category
sodium restriction
pottisum intake adjustment
phosphorous intake adjustment

28
Q

medication management

A

for renally cleared drugs - adjust dosing based on patients GFR
avoid nephrotoxics
contrast is highest risk in pateints with GFR < 30

29
Q

renal replacement therapy

A

non operative: haemodialysis or peritoneal dialysis
operative: kidney transplatation

30
Q

dialysis indications

A

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
Q

ASCVD risk assessment

A

atherosclerotic cardiovascular disease screening for all patients with CKD
diabetes mellitus screening
screening for hypertension
screening for lipid disorders
cardiovascular risk

32
Q

blood pressure control

A

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
Q

lipid management

A

fasting lipid panel may show dyslipidaemia (high triglycerides are common)
statin therapy for patients >50 or with comorbidities, or for treatment of ASCVD

34
Q

antiplatelet therapy

A

usualy indicated for management of ASCVD
may be considered for primary prevention of ASCVD in high risk individuals

35
Q

screening for CKD complications

A

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
Q

calcidiol

A

total body vit D stores

37
Q

monitoring blood gasses

A

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
Q

coagulation screening

A

normal PT, PTT and platelet count
increased bleeding time due to uraemic platelet dysfunction

39
Q

common acute complications of CKD

A

pulmonary oedema
hyperkalaemia
infection
drug toxicity

40
Q

pulmonary oedema

A

Due to an inability in patients with very low GFR to clear excess fluids

41
Q

hyperkalaemia

A

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
Q

infection as a complication

A

bacteraemia secondary to UTI or pneumonia
IV catheter-related infection
haemodialysis catheter related infection
peritoneal dialysis-associated peritonitis

43
Q

calciphylaxis

A

a rare but potentially life-threatening condition characterized by dermal and subcutaneous arteriolar calcifications that cause painful skin necrosis

44
Q

riisk factors for calciphylaxis

A

Most commonly seen in patients with ESRD who are receiving dialysis
Comorbidities: diabetes mellitus, obesity, CKD-mineral and bone disorder, warfarin therapy

45
Q

clinical features of calciphylaxis

A

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
Q

diagnosis of calciphylaxis

A

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
Q

pathophys of anaemia of chronic kidney disease

A

decrease in synthesis of erythropoeitn
decrease stimulation of RBC production
normocytic, normochronic anaemia

48
Q

management of anaemia in CKD

A

diagnostic studies forr iron deficiency
B12 and folate deficiency
erythropoeitn stimulating agenst
avoid blood transfusions

49
Q

CKD mineral and bone disorders

A

abnormalities in mineral and/or bone metabolism in CKD
renal osteodystrophy refers specifically to issues with bone metabolism due to CKD

50
Q

pathophysiology of CKD mineral and bone disorder

A

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
Q

clinical features of CKD bone and mineral diseaase

A

fractures
bone or periarticular pain
muscular weakness and pain
focal vascular calcification (atherosclerotic plaques)
diffuse vascular calcification

52
Q

treatment of CKD bone and mineral disease

A

normlise phosphate, calcium and PTH levels
dietary phosphate restriction
phosphate binders
treatment of hyperparathyroidism: supplimentation for vit D, calcimimetics, parathyroidectomy (last line)

53
Q

secondary hyperprathyroidism

A

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.

54
Q
A

Internal Med 2023 (51 decks)

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