Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

RENAL > Chronic Kidney Disease & RRT > Flashcards

Chronic Kidney Disease & RRT Flashcards

1
Q

define CKD

A

the presence of kidney damage, manifested by abnormal albumin excretion or decreased kidney function, quantified by measured or estimated GFR that persists for more than three months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

is CKD reversible or irreversible

A

irreversible
- renal tissue replaced by extracellular matrix in response to damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

how is CKD measured

A

by estimated GFR (eGFR)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

how is CKD staged

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is the treatment for proteinuria

A

ACE inhibitors or ARb
decrease hydrostatic pressure pushing protein through

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what are the primary causes of CKD

A
  • polycystic kidney disease
  • ATN
  • recurrent pyelonephritis
  • Chronic glomerulonephritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are the secondary causes of CKD (4)

A
  • diabetes mellitus
  • HTN
  • renovascular disease
  • autoimmune
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

80-85% of CKD patients are hypertensive, how is this managed

A

-Anti-hypertensives
-Diuretics
-Fluid restriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

explain why diabetes can result in hyperfiltration and eventually damage to capillaries (CKD)

A
  1. coupled glucose and Na+ reabsorption in PCT so less Na+ in tubule as more glucose being absorbed
  2. this means macula densa cells low Na+ in DCT and activate RAAS
  3. renin and aldosterone released increasing BP
  4. hyperfiltration then occurs which damages capillaries over time
    small amounts of protein will be found in urine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are some risk factors for CKD

A
  • type 2 diabetes: damage to blood vessels due to activation of RAAS (hyperfiltration of RAAS)
  • hypertension: more pressure on glomerulus, too much for regulatory mechanisms to control
  • renovascular disease: narrowing of arteries supplying kidneys
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

describe the gross pathology seen in CKD

A

severe atrophy of medulla and cortex of kidney with the collecting system mostly spared

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

how is diabetes monitored in a pt w CKD

A

fasting plasma glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

why is HbA1C not used to monitor diabetes in pt w CKD

A

in CKD patients, EPO is not produced so patient may be anaemic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are the complications of CKD

A
  • anaema: due to lack of EPO production
  • CKD bone mineral disease
  • hypertension secondary to chronic intravascular volume overload
  • accelerated atherosclerosis/vascular disease
  • metabolic acidosis
  • CVD - No.1 cause of mortality
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

why can you not just give EPO replacements in CKD

A

need iron in order for EPO to make RBC
EPO = builder
iron = building blocks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

which diuretic is the most appropriate to treat fluid overload secondary to CDK stage 4

A

loop diuretic
inhibits Na+K+Cl- co transporter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

why do patients often develop anaemia as a result of CKD

A
  • kidney disease: accumulation of uremic toxins e.g. IS, PCS
  • decreased EPO
  • decreased erythropoiesis in bone marrow
  • decreased RBC production = anaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

why do patients with CKD often develop bone mineral disease and hence non bone calcification

A
  • reduced kidney function means increased plasma PO4- due to less excretion
  • reduced kidney function also means it is unable to activate vitamin D leading to reduced absorption of calcium from gut (low plasma Ca2+)
  • reduction in plasma Ca2+ triggers release of PTH in from parathyroid gland which increases bone resorption and reduces excretion of PO4-
  • large excess of PO4- leads to deposits of calcium phospahate e.g. in blood vessels and joints
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

how does CKD affect the 4 functions of the kidneys (REEM)

A
  1. regulatory
    - cannot control acid/base balance –> acidosis
    - cannot control fluid balance –> fluid overload
    - cannot control PO4 levels –> calcification
  2. excretory
    - conc of urea, Cr, PO4 inc in blood –> uraemia
  3. endocrine
    - not able to produce EPO or activated vitamin D
  4. metabolism
    - reabsorption of glucose
    - drug excretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

a patient has the following complications associated with CKD:
- anaemia
- hypocalcaemia
- hyperphosphatemia
- hyperparathyroidism
- hypertension

how would these conditions be managed

A
  • hypertension –ACEI or ARB, 𝛽-blocker or calcium channel blocker
  • anaemia –If iron deficient then IV iron usually administered. Once iron replete, he should be commenced on recombinant erythropoietin
  • hyperphosphatemia –dietary advice and phosphate binders
  • hypocalcaemia/hyperparathyroidism –provide vitamin D. This will reduce PTH secretion, correct hypocalcaemia
  • Management of traditional vascular risk factors

Aim for Hb 100-120

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is end stage renal failure

A

when death likely without renal replacement
- eGFR < 15

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

when is renal replacement therapy indicated (RRT)

A
  • Required when renal function declines to a level no longer adequate to support health
  • Usually when eGFR 8-10
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what are the 3 types of RRT

A

*Haemodialysis
*Peritoneal dialysis
*Renal transplant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

describe haemodialysis

A
  • using special filters to remove waste that the kidneys can no longer do on their own
  • using mechanisms of diffusion, osmosis and ultrafiltration so that ‘clean blood’ is returned to body
  • The dialysis machine pumps blood from the patient, through disposable tubing, through a dialyser, or artificial kidney, and back into the patient. Waste solute, salt and excess fluid is removed from the blood as it passes through the dialyser
25
Q

what are the pros and cons of haemodialysis

A

pros
- less responsibility
- days off
- proven effective long term

cons
- Dialysis access needs to be secured
* Infection/Bacteraemia
* Haemodynamic instability
* Reactions to dialysers
* Haematomas/risk of bleeding
* Muscle cramps
* Anaemia due to clotted lines/Haemolysis
* AVF steal syndrome
* SVCO from central lines

26
Q

describe peritoneal dialysis

A
  • uses lining of abdomen (peritoneal membrane) to filter blood,
  • catheter in peritoneum surgically placed
  • Solutes (electrolytes, urea, creatinine) move from the patient’s blood, across the peritoneal membrane, down the concentration gradient into the dialysate fluid
27
Q

what are the pros and cons of peritoneal dialysis

A

pros
- continously at home = independence
- less fluid/food restrictions
- easy to travel
- renal function may be better preserved intially

cons
- frequent daily exchanges/overnight
- Unsuitable in patients with stoma/previous surgery
* Risk of infection (PD peritonitis)

28
Q

describe polycystic kidney disease

A
  • Accounts for 8-10% of CKD
  • Most common inherited nephropathy
  • Presentation at 30-40 years of age with complications of hypertension, acute loin pain and/or haematuria or bilateral palpable kidney
  • Cysts develop **anywhere **in the kidney. They compress the surrounding parenchyma and impair renal function
  • Autosomal dominant form affects 1 in 500 to 1000
  • Autosomal recessive affects 1 in 20,000 to 40,000
29
Q

describe the macroscopic appearance of PKD

A

kidneys are large with yellow fluid filled cysts, replacing the parenchyma
- haemorrhage into cysts can occur

30
Q

describe the microscopic appearance of PKD

A

cysts lined by cuboidal epithelium

31
Q

what will an ultrasound or CT of PKD show

A

bilateral enlarged kidneys w multiple cysts

32
Q

describe autosomal dominant PKD and its treatment

A
  • Morbidity and mortality are often the result of hypertension, for example, myocardial infarction and cerebrovascular disease
  • Condition also leads to progressive CKD
  • Treatment involves controlling BP
  • Dialysis and renal transplant are needed if endstage renal failure develops
33
Q

what are some of the clinical manifestations of uraemia

A

brain & CNS
- stroke
- impaired cognition
- anxiet/depression

heart
- heart failure
- palpitations

body fluid
- leg/facial swelling
- high BP
- shortness of breath

digestion
- nausea
- vomiting
- malnutrition
- diarrhoea

skin
- dry skin: pruritus
- brittle nails

34
Q

why is the basement membrane of the glomerulus damaged in diabetic neuropathy

A

high blood pressure (which is caused by hyperfiltration/ renal hypertension)

35
Q

why does hyperfiltration/ renal hypertension happen in diabetic neuropathy

A

hyperglycemia

36
Q

as CKD progresses, what are its clinical features (5)

A
  • Electrolyte disturbances
  • Fluid overload
  • Metabolic acidosis
  • Uraemic pericarditis
  • Uraemic encephalopathy
37
Q

what are the 5 aspects of managing CKD

A
  1. treat underlying disease
  2. reduce CVS risk
  3. reduce progression of CKD
  4. prevent or treat complications of CKD
  5. plan for the future
38
Q

how is the underlying disease treated in CKD

A
  • Treat and monitor diabetic control
  • Treat hypertension
  • Treat infections promptly
  • Tolvaptan if meets criteria for ADPKD
  • Immunosuppression for GN if appropriate
39
Q

how is cardiovascular risk reduced in CKD

A
  • Start on statin
  • Control BP
  • Improve control of diabetes
  • Advise weight loss
  • Advise exercise
  • STOP SMOKING
40
Q

how is disease progression reduced in CKD

A
  • reduce proteinuria - ACEi/ARB
  • monitor blood tests
  • control BP
41
Q

most diabetic patients with CKD will undergo screening for diabetic nephropathy - what evidence are you looking for

A
  • Raised Urine Albumin: Creatinine Ratio/PCR
  • Evidence of long-standing/poorly controlled DM
  • Evidence of other microvascular disease
42
Q

what is hypertensive nephropathy

A

chronic raised BP causing nephrosclerosis

43
Q

what investigations are indicated to identify if primary or secondary HTN (5)

A
  • 24 hour Urinary metanephrines (Phaeochromocytoma)
  • Aldosterone: Renin ratio (Primary aldosteronism)
  • Cortisol & Dexamethasone suppression test (Cushing’s syndrome)
  • TSH (hyperthyroidism)
  • MRA (Renal artery stenosis)
44
Q

what can cause anemia in CKD

A
  • Decreased production of erythropoietin from the kidney
  • reduced absorption of Fe
  • Absolute iron deficiency (poor absorption and malnutrition)
  • Functional iron deficiency (inflammation, infection)
  • Blood loss
  • Shortened Red Blood Cell survival
  • Bone marrow suppression from uraemia
  • Medication induced
  • Deficiency of Vit B12 and folate
45
Q

what are blood results of CKD

A
  • increased ALP & PTH
  • increased phosphate
  • decreased serum Ca2+ & vitamin D
46
Q

what are the 3 types of peritoneal dialysis

A
  • automated
  • continuous ambulatory
  • assisted automated
47
Q

describe features of automated PD

A
  • Carried out with an automated cycler machine performed at night
  • 10-12L usually exchanged, over 8-10 hours
  • Lifestyle advantages – Leaves the daytime free
48
Q

describe features of continous ambulatory PD

A
  • Usually consisting of 4-5 dialysis exchanges per day (usually 2 litres each)
  • Exchanges are performed at regular intervals throughout the day, with a long overnight dwell
49
Q

when is active conservative management considered

A

Decision made after discussion with patient and family members – often after multiple clinic visits and after patient is fully informed of risks & benefits of each mode of therapy

Evidence suggests that if
* Age >80 OR
* WHO performance score of 3 or more
…then RRT offers no survival benefit Often these patients may be unsuitable for or choose to not have invasive therapy such as PD/HD/Transplantation

50
Q

how is an osmotic gradient created in peritoneal dialysis

A

Osmotic gradient is created by high concentration of glucose (occasionally amino acid or glucose polymer solutions are used) in the dialysate fluid, which removes water from the patient

51
Q

what are extra-renal manifestations of ADPKD

A
  • liver cysts (most common) - may cause hepatomegaly
  • berry aneurysms: rupture can cause subarachnoid haemorrhage
  • cvs: mitral valve prolapse, aortic dissection
52
Q

what type of anemia is present in CKD

A

normochromic normocytic anaemia
- becomes apparent when eGFR < 35ml/min

53
Q

what does anaemia in CKD predispose a patient to

A

left ventricular hypertrophy - x3 increase in mortality in renal patients

54
Q

how does reduced absorption of Fe lead to anaemia in CKD

A
  • in CKD there are raised hepcidin levels (acute phase reactant) due to inflammation and reduced renal clearance
  • leads to decreased Fe absorption from gut and impaired release of stored Fe from macrophages and hepatocytes
  • reduced Fe available for erythropoiesis
55
Q

what are some of the clinical manifestation of bone disease as a result of CKD

A
  • osteitis fibrosa cystica (hyperparathyroid bone disease)
  • adynamic
  • osteomalacia due to low vitamin D
  • osteosclerosis
56
Q

what are the complications of peritoneal dialysis

A
  • peritonitis
  • sclerosing peritonitis
57
Q

what procedure do patients need to undergo prior to starting dialysis

A

AV fistual at least 8 weeks before treatment

58
Q

what are complications of haemodialysis

A
  • infection
  • endocarditis
  • stenosis at site
  • hypotension
  • arrhythmia
59
Q

what is the most common cause of peritonitis secondary to peritoneal dialysis

A

Staphylococcus epidermidis is a common cause due to its ability to form biofilms on dialysis catheters

RENAL (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions