Brainscape's Knowledge GenomeTM

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


See full index

My Phase 2a > Renal Diseases > Flashcards

Renal Diseases Flashcards

1
Q

What is acute kidney injury?

A

Rapid deterioration of renal function

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

What are the clinical features of acute kidney injury?

A 
Nausea or vomitting
Diarrhoea
Dehydration
Oliguria (Less urine output)
Confusion
Drowsiness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the types of acute kidney injury?

A

Pre-renal= Impaired perfusion of the kidneys
Renal= Damage to the kidney apparatus
Post renal= Urinary outflow obstructed

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

Which type of AKI is the most common?

A

Pre-renal

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

What causes pre-renal AKI?

A

Volume depletion by vomitting or diarrhoea, hypotension, cardiac failure, sepsis, some medications

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

What causes renal AKI?

A

Glomerular disease like glomerulonephritis, tubular injury, nephritis

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

What causes post-renal AKI?

A

A blockage from something such as an enlarged prostate or kidney stones

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

What is the epidemiology of AKI?

A

15% of adults admitted to hospital develop AKI, more common in the elderly

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

What are the risk factors for AKI?

A

Over 65
Being dehydrated
Severe infection or sepsis
Blockage in the urinary tract
Pre-existing kidney problems
Long-term disease such as heart failure, diabetes, liver disease
Certain medications such as NSAIDs, blood pressure medications, aminoglycosides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How is AKI diagnosed?

A

Usually diagnosed with GFR test for creatinine levels. Serial creatinine readings= Acute rise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How is AKI treated?

A

Treat underlying cause

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

What are some possible complications of AKI?

A

Volume overload

Metabolic acidosis

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

What is chronic kidney disease?

A

An overall term for loss of kidney functions

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

What is stage G1 CKD?

A

A normal GFR but other tests have detected kidney damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is stage G2 of CKD?

A

GFR of 60-89 ml/min, with other signs of kidney damage

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

What is stage G3a of CKD?

A

GFR of 45-59 ml/min

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

What is stage G3b of CKD?

A

GFR of 30-44 ml/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is stage G4 of CKD?

A

GFR of 15-29 ml/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is stage G5 of CKD?

A

GFR below 15ml/min, almost complete loss of function

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

What is stage A1 of CKD?

A

ACR of <3mg/mmol

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

What is stage A2 of CKD?

A

ACR of 3-30 mg/mmol

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

What is stage A3 of CKD?

A

ACR of >30 mg/mmol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Why is there anaemia in CKD?

A

Reduce erythropoietin and increased blood loss

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

Why is there bone disease in CKD?

A

Renal phosphate retention and impaired 1,25-Vit D production, leads to a fall in serum calcium, so release of PTH, so skeletal decalcification

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

What are the clinical features of CKD?

A
  • Oedema of ankles, feet and hand
  • Shortness of breath
  • Nausea, vomitting, diarrhoea
  • Anaemia- pallor lethargy
  • Confusion, Coma
  • Hypertension
  • Nocturia, polyuria, haematuria
  • Osteomalacia, bone pain, hyperparathyroidis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the aetiology of CKD?

A

Polycystic kidney disease, tuberous sclerosis, glomerular disease, urinary tract obstruction, diabetes, kidney infections, NSAIDs

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

What is the epidemiology of CKD?

A

Common. Increases with age

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

What are the main treatments for CKD?

A
  • Lifestyle changes
  • Antihypertensives
  • Dialysis
  • Kidney transplant
  • Vit D supplements and bisphosphonates
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How is CKD diagnosed?

A
  • Abnormalities on scans and histology
  • History
  • Blood tests: Serum calcium, phosphate and uric acid, anaemia
  • GFR: Assess renal function
  • ACR
  • Dipstick: Haematuria, albuminuria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are some possible complications of CKD?

A

Hypertension, renal osteodystrophy, uraemic encaphalopathy, dialysis amyloid deposition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the epidemiology of ADPKD?

A

Commonest inherited kidney disease
Autosomal dominant with high penetrance
Usually presents in adulthood
More common in males

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What causes ADPKD?

A

Mutations in PKD1 (85%) on chromosome 16

Mutations in PKD2 (15%) on chromosome 4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are the risk factors for ADPKD?

A

Family history, ESRF, or hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Briefly explain the pathophysiology of ADPKD

A

PKD1 encodes polycystin 1 which regulates tubular and vascular renal development. PKD2 encodes polycystin 2 which functions as a calcium channel. The polycystin complex occurs in cilia that are responsible for sensing tubular flow. Disruption of the polycystin pathway results in reduced cytoplasmic calcium, which in principle cells causes defective ciliary signalling, and disorientated cell division, leading to cyst formation. This then leaves to apoptosis of healthy tissue and fibrosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the clinical presentation of ADPKD?

A

Can be clinically silent for many years.
Loin pain, haematuria, excessive water and salt loss, nocturia, renal enlargement, hypertension, kidney stones
Polycystic liver disease, Pancreatitis, haemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How is ADPKD diagnosed?

A

Personal history
Family history
Raised blood pressure
Ultrasound= More than 4 cysts per kidney if over 60, more than 2 cysts per kidney if over 40, more than 3 cysts overall if over 15
Genetic testing for PKD1 however this is difficult to do

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

How is ADPKD treated?

A

No treatment to slow cysts
BP control with ACE inhibitor
Treat stones and give analgesia
Laparoscopic removal of cysts or full nephrectomy
Monitoring of condition with serum creatinine
Screening of family
Counselling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is the epidemiology of ARPKD?

A

Rarer that ADPKD
Autosomal recessive inheritance
Disease in infancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is the aetiology of ARPKD?

A

PKHD1 mutation on long arm (q) of chromosome 6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are the risk factors for ARPKD?

A

Family history

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is the differential diagnosis of ARPKD?

A

ADPKD, Multicystic dysplasia, renal vein thrombosis, hydronephrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is the clinical presentation of ARPKD?

A

Variable
Many present in infancy with renal cysts and congenital hepatic fibrosis
Enlarged polycystic kidneys
30% Develop kidney failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

How is ARPKD treated?

A
  • Laproscopic removal of cysts/ full nephrectomy
  • BP control w ACE inhibitor
  • Treat stones and analgesia
  • Renal replacement therapy for ESRF
  • Counselling and support
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

How is ARPKD diagnosed?

A
  • Diagnosed antenatally or neonatally
  • Ultrasound- to view cysts
  • CT and MRI to monitor liver disease
  • Genetic testing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is the epidemiology of minimal change disease?

A
  • Commonest cause of nephrotic syndrome in children
  • Most common in boys under 5
  • Accounts for 20% of adult nephrotic syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What are the clinical features of minimal change disease?

A
  • Proteinuria
  • Oedema (Often in face)
  • Fatigue
  • Frothy urine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are the risk factors/aetiology of minimal change disease?

A
  • Can be idiopathic
  • Atopy is present in 30% of cases and allergic reactions can trigger nephrotic’s syndrome
  • Drugs: NSAIDs, lithium, antibiotics, bisphosphonates, sulfasalazine
  • Hep C, HIV, and TB
  • Associated with Hodgkins lymphoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Briefly explain the pathophysiology of minimal change disease?

A

Glomeruli appear normal on light microscopy but on electron microscopy, fusion of foot processes of podocytes seen, which is consistent with a disrupted podocyte actin cytoskeleton. Immature differentiated CD35 stem cells appear to be responsible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

How is minimal change disease diagnosed?

A

Biopsy: Normal under light microscopy, electron microscopy shows fused podocyte foot processes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

How is minimal change disease treated?

A
  • High dose corticosteroids e.g. prednisolone

- Frequent relapse is treated with cyclophosphamide or cyclosporin/tacrolimus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is nephrotic syndrome?

A

Triad of

  • Proteinuria >3.5g/day
  • Hypoalbuminaemia
  • Oedema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is the epidemiology of nephrotic syndrome?

A
  • Relatively rare
  • Diabetes is most common secondary cause
  • Minimal change disease is the most common cause in children and can also cause it in adults
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What is the aetiology of nephrotic syndrome?

A

Primary causes= Minimal change disease, focal segmental glomerulosclerosis, membranous neuropathy
Secondary causes= Diabetes mellitus, amyloid, infections, SLE, RA, Malignancy, Drugs (NSAIDs, gold)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Briefly explain the pathophysiology of nephrotic syndrome

A

Injury to the podocytes= Proteinuria. Severe hyperlipidaemia is often present: liver goes into overdrive due to albumin loss and other protein loss which increases risk of blood clots

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What are the risk factors of nephrotic syndrome?

A

Diabetes mellitus, minimal change disease in children

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What are the differentials for nephrotic syndrome?

A

Congestive heart failure, cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What is the clinical presentation of nephrotic syndrome?

A
  • Normal-mild increase in BP
  • Proteinuria >3.5g/day
  • Normal-mild decrease in GFR
  • Hypoalbuminaemia
  • Frothy urine
  • Pitting oedema of ankles, genitals, abdomen and face
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

How is nephrotic syndrome diagnosed?

A
  • Establish cause= Renal biopsy
  • Urine dipstick= High protein
  • CXR/Renal ultrasound= Pleural effusion
  • Serum albumin= Low
  • BP is normal or mildly increased
  • Renal function= Normal or mildly impaired
  • Serum creatinine, eGFR, lipids and glucose
  • Differential diagnosis testing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

How is nephrotic syndrome treated?

A
  • Reduced oedema: loop diuretics, thiazide diuretics. Fluid and salt retention
  • Reduce proteinuria: ACE inhibitors, ARBS
  • Reduce risk of complications: prophylactics’ anticoagulation with warfarin, reduce cholesterol with statins, treat infections
  • Treat underlying cause
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What are the complications of nephrotic syndrome?

A
  • Susceptible to infections
  • Thromboembolism
  • Hyperlipidaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What is pyelonephritis?

A
  • Infection of the renal parenchyma and soft tissues of renal pelvis and upper ureter
  • Majority caused by UPEC= Uropathogenic E coli
62
Q

What are the main organisms that cause pyelonephritis?

A 
Klebsiella spp.
Ecoli (majority)
Enterococcus spp.
Proteus spp.
Staph spp.
63
Q

What are the risk factors for pyelonephritis?

A
  • Structural renal abnormalities
  • Calculi (Stones)
  • Catheterisation
  • Pregnancy
  • Diabetes
  • Immunocompromised
64
Q

How is pyelonephritis diagnosed?

A
  • Tender loin on examination
  • Urine dipstick= Nitrates, leucocyte elactase, protein, and foul smelling urine
  • Midstream urine microscopy, culture and sensitivity= Gold standard
  • Bloods= FBC for increased WCC, or Increased CRP/ESR
  • Urgent ultrasound= detects calculi, obstruction, abnormal anatomy
65
Q

What is the epidemiology of pyelonephritis?

A
  • Predominantly affects females under 35
  • Associated with sepsis and systemic upset
  • Mainly caused by UPEC
66
Q

What are the differentials of pyelonephritis?

A

Diverticulitis, abdominal aortic aneurysm, kidney stones, cystitis, prostatitis

67
Q

What are the clinical features of pyelonephritis?

A
  • Triad of loin pain, fever and pyuria
  • May have severe headache
  • Rigors
  • Significant bacteruria
  • Malaise, nausea, vomitting
  • Oliguria if cause is AKI
68
Q

How is pyelonephritis treated?

A
  • Rest
  • Cranberry juice and lots of fluids
  • Analgesia
  • Antibiotics= Oral ciprofloxacillin or oral co-amoxiclav. If severe, IV gentamicin or IV co-amoxiclav
  • Surgery to drain abcesses or relieve calculi that are causing infection
69
Q

What are the characteristic features of acute nephritis syndrome?

A

Haematuria, proteinuria, hypertension and oedema

70
Q

What are the possible causes of acute nephritis syndrome?

A
  • Post strep infection
  • SLE
  • Systemic sclerosis
  • ANCA associated vasculitis
  • Goodpasture syndrome
  • IgA nephropathy (Commonest)
71
Q

How is acute nephritis syndrome diagnosed?

A
  • Take history to determine cause
  • Measure eGFR, Proteinuria, serum U&E, Albumin
  • Culture= throat/skin swab
  • Urine dipstick= Proteinuria, and haematuria
  • Renal biopsy if needed
72
Q

What is the epidemiology of renal cell carcinoma?

A
  • Most common renal tumour in adults
  • Accounts for 2-3% of all malignancies
  • More common in males
  • Usually presents after 50 yrs
  • Highest incidence is in Czechia
73
Q

What are the risk factors for renal cell carcinoma?

A
  • Smoking
  • Obesity
  • Hypertension
  • Polycystic kidney disease
  • Renal failure and haemodialysis
  • Von hippel lindau syndrome
74
Q

What are the clinical features of renal cell carcinoma?

A
  • Often asymptomatic
  • Haematuria, loin/flank pain, abdominal mass
  • Anorexia, malaise and weight loss
  • Rarely, invasion of left renal vein causes compression of left testicular vein causing varicocele
  • Polycythaemia in 5%
  • Hypertension in 30%
  • Anaemia due to low EPO
  • Fever in 20%
75
Q

How is renal cell carcinoma diagnosed?

A
  • Ultrasound to distinguish cyst from tumour
  • CT of chest and abdomen with contrast to show renal mass, renal vein involvement and kidney function
  • MRI for staging
  • Blood pressure
  • Bloods= FBC for polycythamia and anaemia, increased ESR, Abnormal liver biochemistry
  • Renal biopsy and bone scan if needed
76
Q

How is renal cell carcinoma treated?

A
  • Localised disease is treated with surgery
  • Ablative techniques such as cryoablation and radiotherapy
  • Interleukin-2 and interferon alpha
77
Q

What is renal cell carcinoma?

A
  • Malignant cancer of the proximal convoluted tubules epithelium
  • Spread may be direct (Via renal vein), via lymph or haematogenous
78
Q

What is Wilm’s tumour?

A
  • Childhood tumour of the primitive renal tubules and mesenchymal cells
79
Q

What are the clinical features of Wilm’s tumour?

A
  • Abdominal mass

- Haematuria

80
Q

How is Wilm’s tumour diagnosed?

A
  • Ultrasound, CT and MRI
81
Q

How is Wilm’s tumour treated?

A
  • Nephrectomy
  • Radiotherapy
  • Chemotherapy
82
Q

Where are the classical places that renal stones form?

A
  • Pelviureteric junction
  • Pelvic brim
  • Vesicoureteric junction
83
Q

What are the risk factors for renal stones?

A
  • Anatomical abnormalities
  • Chemical composition of urine
  • Dehydration
  • Infection
  • Hypercalcaemia, hyperoxaluria, hyperuricaemia
  • Primary renal disease
  • Diet
  • Family history
84
Q

What are the clinical features of renal stones?

A
  • Many asymptomatic
  • Haematuria
  • Renal colic; sudden severe pain in the loin which travels to the groin. More painful is the stone is moving. Nausea and vomitting
  • Dysuria, strangury, frequency
  • Recurrent UTIs
85
Q

What are the causes of renal stones?

A
  • Calcium; excessive dietary calcium. Excessive bone resorption
  • Uric acid; Hyperuricaemia (gout)
  • Cystine stones; Cystinuria (family history)
86
Q

How are renal stones diagnosed?

A
  • First line; Kidney ureter bladder X ray
  • Gold standard; Non contrast CT of kidney, ureter and bladder
  • Chemical analysis of stones
  • Bloods
  • Dipstick for haematuria
87
Q

How are renal stones treated?

A
  • Diclofenac for pain
  • If less than 5mm, spontaneous passage
  • Oral nifedipine or alpha blocker (Tamsulosin) to promote expulsion
  • Extracorporeal shockwave lithotripsy for larger stones
88
Q

what is glomerulonephritis and what causes it

A
  • inflammation the glomerulus
  • immunologically mediated
89
Q

define nephritic syndrome

A
  • a group of symptoms that fits the clinical picture of inflammation within the kidneys.
  • it does not represent a diagnosis or underlying cause + there are no set criteria.
90
Q

what are the features of nephritic syndrome

A
  • haematuria
  • oliguria: reduced urine output
  • proteinuria
  • fluid retention
91
Q

define nephrotic syndrome and its parameters

A
  • a groups of symptoms that indicate underlying disease.
  • criteria for nephrotic syndrome are:
    1. Peripheral oedema
    2. Proteinuria more than 3g / 24 hours
    3. Serum albumin less than 25g / L
    4. Hypercholesterolaemia
92
Q

define glomerulonephritis

A

an umbrella term for inflammation in the glomerulus and the nephron.

93
Q

examples of types of glomerulonephritis

A

Underlying causes of nephritic syndromes:
- IgA nephropathy
- post streptococcal glomerulonephritis
- Goodpastures syndrome
- SLE nephropathy

Underlying causes of nephrotic syndromes:
- minimal change disease
- focal segmental glomerulosclerosis
- membranous nephropathy

94
Q

T/F
interstitial nephritis is a form of glomerulonephritis

A

FALSE
- this is inflammation of the interstitial cells of the kidney
[it in the name]

95
Q

what are most types of glomerulonephritis treated with?

A
  • immunosuppression: steroids
  • hypertension management via the RAAS system: ACEi’s + ARBs.
96
Q

typical presentation of nephrotic syndrome

A
  • peripheral oedema
  • frothy urine -high protein content
97
Q

what does nephrotic syndrome predispose a pt to?

A
  • thrombosis due to hyper coagulability caused by loss of antithrombin 3 in urine
  • hypercholesteraemia
  • hypertension
98
Q

what is the most common underlying cause of nephrotic syndrome in kids and in adults

A
  • kids: minimal change disease
  • adults: focal segmental glomerulosclerosis
99
Q

what is the most common cause of primary glomerulonephritis

A

IgA nephropathy [Berger’s disease]

100
Q

what is IgA nephropathy

A

Deposition of IgA into the mesangium of the kidney. Causes inflammation and damage

101
Q

how does IgA nephropathy present

A

Presents asymptomatically with microscopic haematuria

102
Q

how is IgA nephropathy diagnosed

A
  • urine dipstick: shows blood and protein in the urine
  • biopsy: shows IgA deposits and glomerular mesangial proliferation”.
103
Q

how is IgA nephropathy managed

A
  1. ACEi/ARB for BP control
  2. statins to slow disease progression
  3. steroids - if persitent proteinuria after 3-6 months of ACEi/ARB
  4. omega-3 fatty acids [fish oil] - if persitent proteinuria after 3-6 months of ACEi/ARB
104
Q

complications of IgA nephropathy

A
  • CKD
  • Hypertension
  • Henoch-Schönlein purpura: a small-vessel vasculitis secondary to IgA deposition.
105
Q

systemic causes of nephritic syndrome

A
  • SLE
  • Post Strep GN
  • Goodpasture’s
  • Small vessel vasculitis
106
Q

renal cause of nephritic syndrome

A
  • IgA nephropathy
107
Q

pathophysiology of IgA nepropathy

A
  1. IgA immune complexes deposit in the mesangium of the kidneys
  2. this causes the acrtivation of the alternative compliment pathway –>
  3. glomerular injury.
108
Q

risk factors for IgA nephropathy

A
  • male
  • asian
  • 16-35 yrs
  • presence of other autoimmune conditions
109
Q

what is the most common type of glomerulonephritis condition

A

membranous glomerulonephritis

110
Q

what is membranous glomerulonephritis

A
  • Thickening of glomerular capillary wall.
  • IgG, complement deposit in sub epithelial surface causing leaky glomerulus
111
Q

how is membranous glomerulonephritis diagnosed

A

Renal Biopsy showing:
- thickened basement membrane
- sub-epithelial IgG immune complex deposits.

112
Q

how is membranous glomerulonephritis managed

A
  • corticosteroids + cyclophosphamide
  • ACEi/ARB
  • statin
  • maybe warfarin.
113
Q

what is post strep glomerulonephritis

A

Glomerulonephritis that occurs 1-6 weeks after a strep infection caused by deposition of strep antigens in the kidney –> inflammation and damage
- 1-2 weeks after throat infection
- 2-6 weeks after skin strep infection.

114
Q

T/F
post strep glomerulonephritis is the only renal condition triggered by prior infection

A

False
- IgA nephropathy can also be triggered by an infection and can occur 1-2 weeks after an URTI

115
Q

typical presentation of post strep glomerulonephritis

A
  • acute development of nephritic syndrome:
  • haematuria
  • oliguria
  • hypertension
    [oedema (normally periorbital, due to salt retention in the loose skin).]
116
Q

name all the conditions that can present with a nephritic picture

A

SHARP AIM
* SLE
* Henoch-Schönlein purpura
* Anti glomerular basement membrane (GBM) disease (AKA Goodpasture’s disease)
* Rapidly Progressive glomerulonephritis (GN)
* Post-streptococcal GN
* Alport’s syndrome
* IgA nephropathy
* Membranoproliferative GN

117
Q

management of post strep glomerulonephritis

A
  • ABX to clear infection if still present.
  • supportive management
118
Q

example of a strep infection of the throat and skin

A
  • tonsillitis
  • strep throat
  • impetigo
119
Q

what is Henoch Schoenlein purpura

A

Small Vessel Vasculitis that affects kidneys and joints due to IgA deposition

120
Q

typical presentation of Henoch Schoenlein purpura

A
  1. purpuric rash on legs
  2. nephritic syndrome
  3. joint pain
121
Q

how is Henoch Schoenlein purpura diagnosed

A

renal biopsy: showing IgA deposition

122
Q

T/F
all types of nephritic syndromes are type 3 hypersensitivity reactions

A

FALSE
- they all are except for Goodpasture’s syndrome which is type 2

123
Q

what is Goodpasture’s syndrome

A
  • an autoimmune condition where antibodies are produced against type 4 collagen –> their destruction.
  • the antipodes act against antigens in the glomerular basement membrane and lung alveoli, making this a renal-respiratory condition.
124
Q

typical presentation of Goodpasture’s syndrome

A
  • haematuria macro/microscopic
  • proteinuria
  • haemoptysis + SoB
125
Q

how is Goodpasture’s syndrome diagnosed?

A
  • renal biopsy: shows crescentic glomerulonephritis
  • serology: presence of anti-GBM in the blood
126
Q

management of Goodpasture’s syndrome

A
  • corticosteroids + cyclophosphamide
  • plasma exchange - remove the autoantibodies.
127
Q

key differential for Good pasture’s syndrome.
- key differences

A
  • granulomatosis with polyangiitis (AKA Wegener’s granulomatosis)
  • GPA serology shows ANCA whereas good pasture shows anti-GBM
  • GPA may also present with a wheeze, saddle nose + sinusitis.
128
Q

what is minimal change disease

A

a nephrotic disease where the podocytes fuse together

129
Q

management of minimal change disease

A
  1. steroids
  2. cyclophosphamide
130
Q

what are the ECG findings of hyperkalaemia

A
  • Tall tented T waves
  • Wide QRS
  • Flattening of P wave
  • Prolonged PR interval
131
Q

what are the 4 main continence features

A
  1. Internal sphincter
  2. External sphincter
  3. Pelvic floor muscles
  4. Prostate in men – important in surgery
132
Q

what are the physiological components that control micturition

A
  1. cortex
  2. the pontine micturition centre
  3. the spinal reflexes - onufs nucleus and the sacral mictruition centre
133
Q

role of the nervous system in the process of micturition

A
  • parasympathetic system makes you wee: detrusor contraction and sphincter relaxation [smooth muscle]
  • sympathetic system holds your wee: detrusor relaxation to avoid pressure build up as wee is colleccted + contraction of the internal sphincter [smooth muscle].
  • somatic system lets you control when you wee by controling contraction of striated muscle in the sphincters
134
Q

what are the main classes of LUTS
- what are their features

A
  1. storage
    • frequency
    • urgency
    • nocturia
    • incontinence
  2. voiding
    • Poor flow
    • Intermittency
    • Straining
    • Terminal dribbling
    • Hesitancy
  3. Post-micturition [technically a part of voiding]
    • Sensation of incomplete voiding
    • Post-micturition dribbling
135
Q

what is the cause of storage LUTS

A
  • overactive bladder: hyperstimulation + contraction -> feeling the need to wee all the time
  • enlarged prostate gland: forms a valve that prevents complete bladder emptying -> frequency + nocturia
136
Q

what is the cause of voiding LUTS

A
  • enlarged prostate: due to prostate preventing smooth passage of urine through the urethra.
137
Q

difference between post-micturition dribbling + terminal dribbling

A
  • the timing.
  • post micturition happens after theyv’e pulled up their trousers and more urine comes out
  • terminal dribbling occurs right at the end of urination
138
Q

what causes urinary retention

A
  • masses: tumours in the pelvic region
  • pregnancy
  • enlarged prostate BPH most common
  • urethral stricture [narrowing of urethra]
  • prolapse
  • atonic bladder - non obstructive. no contraction of bladder.
139
Q

what is incontinence

A

the involuntary passage of urine

140
Q

what are the main types of incontinence

A
  • stress incontinence: due to loss of pelvic floor muscle strength, seen in pregnant women or vaginal birth.
  • urge incontinence: unable to make it in time -> wetting yourself.
  • mixed incontinence hard to treat
141
Q

what are the 2 extreme ends of LUTS

A
  • urinary retention: blockage of wee
  • urinary incontinence: cant hold wee
142
Q

what investigations would you do for a pt presenting with LUTS

A
  • U+Es for renal function
  • bloods - eGFR
  • Ultrasound or Ct scan looking for abdominal mass
  • DRE – for prostate enlargement.
  • Flow rate – wee in a funnel to measure speed of urination. Give info on speed of stream
  • Post-wee bladder scan – to see if they fully emptied bladder
  • Bladder diary – how often pt wees and how much wee each time and how much they drink in a day and what they drink too- caffeine ↑ need to wee
143
Q

what is pyuria

A

the presence of pus + leukocytes in the urine, usually due to infection.

144
Q

what is bacteriuria + how does it present

A
  • bacteria in the blood
  • can be a/symptomatic
145
Q

besides infection, what else can cause pyuria

A
  • renal stones
  • cancer
  • renal TB
  • diabetes
146
Q

what is classed as an uncomplicated UTI

A
  • UTI in non-pregnant women
147
Q

T/F
UTI isn’t always complicated in men

A

FALSE
it’s always complicated as men have a longer urethra so the infection is more established men.

148
Q

6 examples of complicated UTIs

A

basically anyone that isn’t a “non-pregnant, healthy woman”
1. preganant
2. male
3. immunocompromised
4. children
5. recurrent / persistent infections
6. catheterised pts

149
Q

most common causative organisms of UTI

A

KEEPS
* Klebsiella
* E.coli - most common
* Enterococci
* Proteus
* Staph. saprophiticus

150
Q

What is the symptomatic triad that Px with pyelonephritis present with

A
  • fever
  • flank pain
  • N+V
151
Q

T/F
you should always treat asymptomatic bacturia

A

FALSE
* only treat inpregnant women
* NEVER treat catheterised OR elderly asymptomatic pts with bacturia

My Phase 2a (35 decks)

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