Brainscape's Knowledge GenomeTM

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


See full index

Renal > Diseases > Flashcards

Diseases Flashcards

1
Q

Define AKI

A

An abrupt (<48hrs) reduction in kidney functions defined as;

  • an absolute increase in serum creatinine by >26.4 micromol/L
  • increase in creatinine by >50%
  • a reduction in UO

note can only be applied following adequate fluid resuscitation and exclusion of obstruction

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

Name patient risk factors for AKI

A
  • older age
  • CKD
  • diabetes
  • cardiac failure
  • liver disease
  • PVD
  • previous AKI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Name exposure risk factors for AKI

A
  • hypotension
  • hypovolaemia
  • sepsis
  • deteriorating NEWS
  • recent contrast
  • exposure to certain medications
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the three categories of causes of AKI?

A
  • pre-renal (functional|)
  • renal (structural)
  • post renal (obstruction)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Name pre-renal causes of AKI

A
  • hypovolaemia; haemorrhage, volume depletion (e.g. D&V, burns)
  • hypotension; cardiogenic shock, distributive shock (e.g. sepsis, anaphylaxis)
  • renal hypoperfusion; NSAIDs/ COX2, ACEi / ARBs, hepatorenal syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the basic pathogenesis of pre-renal AKI?

A

Reversible volume depletion leading to oliguria and increase in creatinine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Untreated pre-renal AKI can lead to what?

A

Acute tubular necrosis (histological diagnosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the commonest form of AKI in hospital?

A

Acute tubular necrosis

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

Name causes of acute tubular necrosis

A
  • due to a combination of factors leading to decreased renal perfusion
  • common causes include sepsis and severe dehydration
  • other important causes include rhabdomyolysis and drug toxicity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe management of pre-renal AKI

A
  • assess for hydration; clinical observations (BP, HR, UO), JVP, cap refill, pulmonary oedema
  • fluid challenge for hypovolaemia;
    > crystalloid (0.9% NaCl) or colloid (gelofusin)
    > do not use 5% dextrose
    > give bolus of fluid then reassess and repeat as necessary
    > if >100mls IN and no improvement seek help
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the basic pathogenesis of renal AKI?

A
  • diseases causing inflammation or damage to cells causing AKI
  • split by structure; blood vessels, glomerular disease, interstitial injury, tubular injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Name causes of renal AKI

A
  • vascular; vasculitis, renovascular disease
  • glomerular; glomerulonephritis
  • interstitial nephritis; drugs, infection (TB), systemic (sarcoid)
  • tubular injury; ischaemia (prolonged renal hyperfusion), drugs (genatmicin), contrast, rhabdomyolysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Name signs and symptoms of renal AKI

A
  • Non specific symptoms
  • constitutional; anorexia, weight loss, fatigue, lethargy
  • nausea and vomiting
  • itch
  • fluid overload; oedema, SOB

Signs

  • fluid overload including HTN, oedema, pulmonar oedema, effusions
  • uraemia including itch, pericarditis
  • oliguria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Name initial investigations for AKI

A
  • U&Es; marker of renal function (Na, K, Ur, Cr), look at potassium
  • FBC and coagulation screen; abnormal clotting, anaemia
  • urinalysis; haematoproteinuria
  • USS; ?obstruction ? size
  • immunology; ANA, ANCA, GBM
  • protein electroporesis and BJP (? myeloma)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe treatment of renal AKI

A
  • establish good perfusion pressure; fluid resuscitate, once fluid restricted, if still not achieving adequate BP > inotropes/ vasopressors
  • treat underlying cause; antibiotics if sepsis
  • stop nephrotoxics
  • dialysis if remains anuric and uraemia; can require urgent dialysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Name the life threatening complications of AKI

A
  • hyperkalaemia
  • fluid overload
  • severe acidosis (pH <7.15)
  • uraemic pericardial effusion
  • severe uraemia (Ur >40)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe the basic pathogenesis of post renal AKI

A
  • AKI due to obstruction of urine flow leading to back pressure (hydronephrosis) and thus loss of concentrating ability
  • causes; stones, cancers, strictures, extrinsic pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Describe treatment of post renal AKI

A
  • relieve obstruction; catheter, nephrostomy (blockage further up)
  • refer to urology is ureteric stenting required
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What value of potassium is;
A) normal
B) hyperkalaemia
C) life threatening hyperkalaemia

A

A) 3.5 - 5.0
B) >5.5
C) >6.5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How is hyperkalaemia assessed (other than biochem)?

A
  • ECG

- muscle weakness

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

What changes are seen on ECG for hyperkalaemia

A
  • peaked / tented T waves
  • flattened P wave
  • prolonged PR interval
  • ST depression
  • sine wave pattern if severe
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Describe medical management of hyperkalaemia

A
  • cardiac monitor and IV access
  • protect myocardium; 10mls 10% calcium gluconate (2-3mins)
  • move K+ back into the cells; insulin (actrapid 10units) with 50mls 50% dextrose (30mins), salbutamol nebuliser (90mins)
  • prevent absorption from GI tract; calcium resoniu (not in the acute setting)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Name indicated for urgent haemodialysis

A
  • hyperkalaemia; >7 or >6.5 unresponsive to medical therapy
  • severe acidosis; pH <7.15
  • fluid overload
  • urea >40, pericardial rub / effusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

40 year old male, presenting with general malaise and haemoptysis Urea is 28, creatinine 600, elevated ant-GBM) is a typical history of what?

A

Goodpastures syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

25 year old PWIJ found collapsed at home is a history typical of what?

A

Rhabdomyolosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

82 year old man admitted with BP 70/30, T 39, HR 140BPM, K+ 7.0, urea 48, Cr 789, CRP 250, CXR left basal consolidation is a history typical of what?

A

Acute tubular necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

72 year old man presenting with difficulty passing urine and reduced urine output is a history typical of what?

A

Obstructive uropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Name drugs that can cause hyperkalaemia

A
  • spironolactone
  • ramipril
  • amiloride
  • atenolol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the two types of polycystic kidney disease?

A
  • autosomal dominant (most common)

- autosomal recessive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Describe autosomal dominant polycystic disease

A
  • ADPKD is the most frequent life threatening hereditary kidney disease
  • occurs worldwide and in all races and ethnic groups
  • an important cause of ESRD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the common mutations in ADPKD?

A
  • mutations in PKD gene 1 located on chromosome 16 (85% of cases)
  • PKD2 mutation located on chromosome 4 (15% of cases)
  • PKD1 patients develop end stage kidney failure at an earlier stage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Describe the pathology of ADPKD

A
  • massive cyst enlargement > large kidneys
  • epithelial lined cysts arise from a small population of renal tubules
  • benign adenomas = 25% of kidneys
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Describe the renal features of ADPKD

A
  • reduced urine concentration ability
  • chronic pain
  • hypertension; common, early (31 yrs old mean age)
  • haematuria; cyst rupture, cystitis, stones
  • cyst infection (difficult to treat)
  • renal failure
34
Q

Describe the extra-renal features of ADPKD

A
  • hepatic cysts; most common. present 10 yrs after renal cysts, liver function generally preserves, can result in SOB, pain, ankle swelling
  • intra-cranial aneurysms; seen in clusters of family members, mainly in the anterior circulatory territory, screen if +ve family history
  • cardiac disease; mitral/ aortic valve prolapse, valvular disease
  • diverticular disease; diverticulitis and colonic perforation
  • hernias; abdominal / inguinal hernias
35
Q

Describe the diagnosis of ADPKD

A
  • radiologic; ultrasound presence of multiple bilateral cysts, renal enlargement, CT/MRI when unclear on USS
  • genetic; linkage analysis, mutation analysis
36
Q

Describe ADPKD in children

A
  • early onset, can be in utero or first year of life
  • siblings at increased risk of early disease
  • renal involvement similar to adults
  • a single cyst in high risk pts is enough for diagnosis
  • cerebral aneurysms rare in children
37
Q

Describe management of ADPKD

A
  • hypertensions rigorous control
  • hydration
  • proteinuria reduction
  • cyst haemorrhage and cyst infection treated
  • tolvaptan (ADH receptor antagonist)
  • renal failure; dialysis, transplantation
38
Q

Describe autosomal recessive kidney disease

A
  • young children and associated with hepatic lesions
  • rare
  • renal involvement is bilateral and symmetrical
  • urinary tract is generally normal
  • histologically cysts are seen appearing from the collecting duct system
39
Q

Describe the clinical presentation of ARPKD

A
  • varies and depends on the renal / liver lesions
  • relevance is distinguishing between severe forms and ones which survive the neonatal period
  • kidneys always palpable
  • hypertension
  • recurrent UTIs
  • slow decline in GFR; less than 1/3 reach dialysis
40
Q

What is alports syndrome

A
  • hereditary nephritis
  • familial glomerular syndrome
  • 1-2% pts with ESRD
  • x linked inheritance
  • disorder of type 4 collagen matrix
  • mutation in COL4A5 gene leads to deficient collagenous matrix deposition
41
Q

Describe the manifestations of alports syndrome

A
  • haematuria; characteristic feature
  • proteinuria seen later but confers bad prognosis
  • extra renal; sensorineural deafness, ocular defects (anterior lenticonus), leiomyomatosis of oesophagus / genitalia rare
42
Q

Describe the diagnosis of alports

A
  • suspected in patients with microscopic haematuria +/- hearing loss
  • renal biopsy; variable thickness (GBM characteristic feature)
43
Q

Describe the treatment of alports

A
  • no specific treatment
  • standard aggressive treatment of BP, proteinuria
  • dialysis / transplantation
44
Q

What is anderson fabrys disease?

A
  • inborn error of glycosphingolipid metabolism (deficiency of alpha-galactosidase A)
  • x linked disease lysosomal storage disease
  • affects kidneys, liver, lungs, erythrocytes
  • uncommon
45
Q

Describe the clinical features of anderson fabrys disease

A
  • renal failure
  • cutaneous; angiokeratomas
  • cardiac; cardiomyopathy, valvular disease
  • neuro; stroke, acroparaesthesia
  • psychiatric
46
Q

Describe the diagnosis of fabrys disease

A
  • plasma / leukocyte a-GAL activity
  • renal biopsy
  • skin biopsy
  • concentric lamellar inclusions with lysosomes - pathognomic
47
Q

Describe the treatment of anderson fabrys disease

A
  • enzyme replacement - fabryzyme

- management of complications

48
Q

What is medullary cystic kidney?

A
  • rare inherited cystic disease, autosomal dominant
  • morphologically abnormal renal tubules leading to fibrosis
  • affected; normal / small kidneys
  • cysts are in the corticomedullary junction / medulla (not essential for diagnosis)
49
Q

What is the macroscopic appearance of medullary cystic kidney?

A
  • cortex and medulla are both shrunken

- presence of irregularly distributed cysts of variable size at the corticomedullary junction and in the outer medulla

50
Q

Describe the diagnosis and treatment of medullary cystic kidney

A
  • diagnosis; family history, ct scan
  • presents average age 28 years
  • renal transplantation
51
Q

Describe medullary sponge kidney

A
  • uncommon
  • sporadic inheritance
  • dilatation of collecting ducts
  • severe cases; medullary are appears like a sponge
  • cysts have calculi
  • diagnosis is by excretion urography; to demarcate calculi
  • renal failure unusual
52
Q

Define CKD

A

A reduction in kidney function or structural damage (or both) present for more than 3 months, with associated health implications

53
Q

CKD should be diagnosed in people with markers of kidney damage such as?

A
  • a urinary albumin:creatinine ratio (ACR) greater than 3mg/mmol
  • urine sediment abnormalities
  • electrolyte and other abnormalities due to tubular disorders
  • abnormalities detected by histology
  • structural abnormalities detected by imagine
  • a history of kidney transplantation

and / or
- a persistent reduction in renal function shown by a serum eGFR of less than 60ml/min/1.73m2

54
Q

Define accelerated progression of CKD

A
  • a persistent decrease in eGFR of 25% or more AND a change in CKD category within 12 months

or

  • a persistent decrease of eGFR of 15mL/min/1.73m2 within 12 months
55
Q

Name causes of CKD

A
  • conditions associated with intrinsic kidney damage such as; hypertension, diabetes, glomerular disease
  • current or previous AKI
  • potentially nephrotoxic drugs
  • causes of obstructive uropathy such as; structural renal tract disease, neurogenic bladder, benign prostatic hypertrophy, malignancy (bladder, prostate, ureteric), urinary diversion surgery, recurrent urinary tract calculi
  • SLE, vasculitis, myeloma
  • a Fhx of CKD stage 5
56
Q

Renal anaemia may present with what?

A
  • symptoms such as tiredness, shortness of breath, lethargy and palpitations
  • may be due to reduced productions of erythropoietin by the kidney, reduced red blood cell survival and iron deficiency
57
Q

Describe how renal mineral and bone disorder may present

A
  • this may present with bone pain, increase bone fragility, or extra skeletal calcification such as in the skin or blood vessels
  • give exogenous vitamin D
58
Q

Peripheral neuropathy and myopathy may present with what?

A
  • paraesthesia, sleep disturbance and restless legs syndrome
59
Q

What is the initial treatment of CKD?

A
  • treat the underlying condition
  • diabetes > HbA1c target
  • hypertension
  • autoimmune / multisystemic conditions
  • obstruction; relieve it
  • nephrotoxins; stop
60
Q

What is the blood pressure aims for CKD and CKD with diabetes?

A

CKD alone

  • systolic below 140mmHg
  • diastolic below 90mmHg

CKD and diabetes; (also in people with an ACR of 70mg/mmol or more)

  • systolic below 130 mmHg
  • diastolic below 80mmHg
61
Q

What dietary advice is given to patients with CKD?

A
  • phosphate restriction (if PO4 is high)
  • salt reduction
  • potassium restriction (if persistently elevated)
  • fluid restriction to 1 - 1.5l per day
62
Q

Describe the investigation and management of anaemia in CKD

A
  • exclude other causes of anaemia
  • check ferritin and iron stores, aiming for; ferritin >100, TSats >20%
  • IV iron therapy; ferric carboxymaltose, iron sucrose
63
Q

Name common presenting symptoms of kidney disease

A
  • asymptomatic
  • loin pain / urinary symptoms
  • haematuria; microscopic, painless macroscopic
  • proteinuria
  • hypertension; asymptomatic, accelerated
  • AKI
  • chronic kidney disease
  • nephrotic sndrome
  • nephritic syndrome
64
Q

What is a transplant?

A
  • tissue taken from one person and placed in another

- either be taken from someone who has died or from a living donor

65
Q

Name the different types of transplant

A
  • decreased heart beating donors; brain stem death (DBD)
  • non heart beating donors (DCD)
  • live donation; directed and undirected, paired donation, financially procured
66
Q

How are patients assessed for transplantation?

A
  • immunology; tissue typing and antibody screening
  • virology (exclude active infection)
  • assess cardiorespiratory risk; ECG, echo, CXR etc
  • assess peripheral vessels
  • assess bladder function
  • assess mental state
  • assess any co-morbidity / PMHx which may influence transplant or be exacerbated by immunosuppression
67
Q

Name some contraindications to transplant

A
  • malignancy; known untreated malignancy, solid tumour in last 2- 5 yrs
  • active HCV/HIV infection
  • untreated TB
  • severe IHD, not amenable to surgery
  • severe airways disease
  • active vasculitis
  • severe PVD
  • hostile bladder
68
Q

What factors are looked at for tissue typing?

A
  • blood group

- HLA A , B and DR

69
Q

Name examples of sensitising events for transplant

A
  • blood transfusion
  • pregnancy or miscarriage
  • previous transplant
70
Q

How can patients be desensitised for transplantation?

A
  • active removal of blood group or donor specific antibody
  • plasma exchange
  • and /or b cell antibody (rituximab)
71
Q

Describe the transplant procedure

A
  • extra peritoneal procedure
  • transplant inserted in iliac fossa; attached to external iliac artery and vein, ureter plumbed into bladder with stent
  • wound 15-20cm long
  • average 2-3 hr operation
  • 7-10 days in hospital
72
Q

Name surgical complications of transplant

A
  • bleeding
  • arterial stenosis
  • venous stenosis / kinking
  • ureteric stricture and hydronephrosis
  • wound infection
  • lymphocele
73
Q

Name the different types of rejection

A
  • hyperacute rejection; due to preformed antibodies, unsalvageable, transplant nephrectomy require, should be a never event
  • acute rejection; cellular or antibody mediated, can be treated with increased immunosuppression
  • chronic rejection; antibody mediated slowly progressive decline in renal function. Poorly responsive to treatment
74
Q

Describe immunosuppressive therapy

A
  • induction treatment; basiliximab / dacluzimab
  • prednisolone IV during operation
  • maintainance treatment; prednisolone, tracrolimus, MMF or prednisolone, ciclosporin, azathioprine
75
Q

Name anti-rejection treatments

A
  • pulsed IV methylprednisolone (ACR)
  • anti thymocyte globulin (ATG), (resistance ACR and AMR)
  • IV immunoglobulin (AMR)
  • plasma exchange (AMR)
  • rituximab, bortezimab, eculizumab (AMR)
  • intensification of immunosuppression
76
Q

Describe CMV disease as a complication of transplant

A
  • important cause of morbidity in immunosuppressed patients in first 3 months
  • associated with early graft loss
  • common if recipient is not immune but donor has evidence of previous infection
  • causes; renal and hepatic dysfunction, oesophagitis, pneumonitis and colitis, increased risk of rejection
  • evidence; IgM and PCR+ve
  • treatment; prophylactic PO valganciclovir in higher risk patients, IV ganciclovir if evidence of infection
77
Q

Describe BK nephropathy as a complication of transplantation

A
  • prevalent and indolent in uroepithelium
  • reflection of over immunosuppression
  • can mimic rejection
  • no effective anti-viral therapy
  • treat by reducing immunotherapy
  • monitor blood viral load by PCR
78
Q

Name the commonest malignancies that occur due to complications of transplantation

A
  • non melanoma skin cancers
  • lymphoma (e.g EBV mediated PTLD)
  • solid organs
79
Q

Describe post transplant lymphoproliferative disease

A
  • occurs in all forms of transplantation
  • depends on immunosuppression level
  • usually related to EBV infection
  • reduce immunosuppression
  • chemotherapy
  • no role for antiviral therapy
80
Q

Name causes of graft loss

A
  • acute rejection
  • death with a functioning graft
  • recurrent disease
  • chronic allograft nephropathy
  • viral nephropathy
  • PTLD

Renal (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions