Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

3B General Care > Nephrology > Flashcards

Nephrology Flashcards

1
Q

focal

A

some but not all glomeruli contain the lesion

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

diffuse (global)

A

most glomeruli contain the lesion

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

Segmental

A

only a part of the glomerulus contain the lesion (often focal as well)

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

proliferative

A

an increase in cell numbers due to hyperplasia of one or more of the resident glomerular cells with or without inflammation

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

membrane alterations

A

capillary wall thickening due to deposition of immune deposits or alterations in the basement membrane

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

Nephrotic syndrome

What is is?

A

Increased filtration of macromolecule across the glomerular capillary wall
- due to structural and functional abnormalities of glomerular podocytes

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

Clinical features of nephrotic syndrome

A
  1. Hypoalbuminaemia - as a result of heavy proteinuria & increased renal catabolism of filtered protein
  2. Oedema - due to sodium retention & increased capilliary permeability
  3. Hypercholesterolaemia & hypertriglyceridae,oa - increased synthesis and impaired catabolism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Aetiology

Membranous nephrotic syndrome

A
  • idiopathic
  • drugs (gold, penicillamine, NSAIDs)
  • autoimmune ( SLE, thyroiditis)
  • Neoplasia
  • Infections

–> IgG deposition & complement C3 in the outer glomerular basement membrane

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

Clinical features of nephrotic syndrome

A

Oedema of the ankles, genitals and abdominal wall

Periorbital oedema and arm oedema may also be features of severe disease

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

Differential diagnosis for nephrotic syndrome

A
  • Congestive cardiac failure (would also be raised JVP)

- cirrhosis (would also be signs of liver failure)

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

Management of nephrotic syndrome

A

General oedema- salt restriction, diuretics & amiloride
Proteinuria - ACE-i/ ARB, normal diet
Specific treatment: (of underlying disease), cyclophosphamide, chlorambucil with prednisolone, rituximab in resistant disease

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

Complications of nephrotic syndrome

A

Venous thrombosis (loss of clotting factors in urine)
Sepsis (loss og Ig in urine increases susceptibility to infection)
AKI (result of progression of underlying renal disease, consequence of hypovolaemia or renal vein thrombosis)

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

Acute glomerulonephritis

A

caused by an immune response triggered by an infection or other disease
typically post strep (group A, beta-haemolytic strep)
Bacterial antigen becomes trapped in the glomerulus leading to acute diffuse proliferative glomerulonephritis

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

Acute glomerulonephritis

clinical features

A
  • haematuria
  • proteinuria
  • hypertension and oedema (periorbital, leg or sacral) caused by salt and water retention
  • oliguria
  • uraemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Management of post strep glomerulonephritis

A

supportive

  • HTN –> salt restriction and loop diuretics & vasodilators
  • Fluid balance & daily weights
  • Fluid restriction if evidence of fluid overload
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Rapidly progressing glomerulonephritis

A
  • anti-glomerular basement disease (with lung involvement = Goodpasture’s syndrome)
  • anti-neutrophilic cytoplasmic antibody (ANCA) vasculitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Pathogenesis of UTI

A

sexual intercourse
urethral catheterisation
cystitis encouraged by urinary obstruction/ stasis, previous damage to bladder epithelium, bladder stones, poor bladder emptying

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

Clinical features of lower UTI

A 
micturition, 
dysuria, 
suprapubic pain and tenderness, 
Haematuria 
Smelly urine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Clinical features of acute pyelonephritis

A

Loin pain & tenderness
Nausea & Vomiting
Fever

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

Acute pyelonephritis

A

neutrophil infiltration of the renal parenchyma

small cortical abscesses & streaks of pus in renal medulla

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

reflux nephropathy

A

childhood UTIs + vesicoureteric reflux –> progressive renal scarring –> hypertension + CKD

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

Recurrent UTI

A

same or different organism more than 2 weeks after stopping abx = reinfection
Relapse = recurrence of bacteriuria with the same organism within 7 days

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

TB of the urinary tract

A

symptoms of UTI

sterile pyuria

Culture of mycobacteria from early morning urine sample

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

Tubulointerstitial nephritis

A

primary injury to renal tubules and interstitium –> decreased renal function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Acute tubulointerstitial nephritis causes
most due to allergic drug reaction (penicillins/ NSAIDs) | Infection less common
26
Presentation of acute tubulointerstitial nephritis
``` fever eosinophila eosinophiluria normal/ mildly raised proteinuria AKI ```
27
Management of acute tubulointerstitial nephritis
withdrawal of causative drug | High dose prednisolone
28
Chronic tubulointerstitial nephritis causes
prolonged consumption of large amounts of analgesia (NSAIDs), DM & toxina
29
Presentation of Chronic tubulointerstitial nephritis
polyuria proteinuria uraemia (polyuria & nocturia are the result of tubular damage --> inability to properly concentrate urine)
30
Bilateral renal disease Renal hypertension
hypertension complicates bilateral renal disease (glomerulonephritis, reflux nephopahty or analgesic nephropathy) - Activation of renin-angiotensin-aldosterone system - Retention of salt and water --> increase in blood volume and therefore blood pressure
31
Renovascular disease
narrowing of renal arteries - usually due to atheroma, but may also be due to fibromuscular hyperplasia - renal perfusion pressure is reduced - renal ischaemia --> reduced pressure in afferent glomerular arterioles
32
Nephrocalinosis
diffuse renal parenchymal calcification painless hypertension and renal impairment commonly occur
33
Nephrocalcinosis causes
Medullary - hypercalcinaemia, renal tubular acidosis, primary hyperoxaluria, medullary sponge kidney, TB Cortical - renal cortical necrosis
34
Renal failure
failure of renal excretory function result of reduction in GFR Accompanied to a variable extent by failure of EP production, Vit D hydroxylation, regulation of acid-base balance & BP control
35
Define AKI
abrupt, sustained rise in serum urea & creatinine due to a rapid decline in GFR - loss of normal water and solute homeostasis
36
Pre-Renal causes of AKI
impaired perfusion of the kidneys - hypovolaemia - hypotension - impaired cardiac pump efficiency - vascular disease ACE-i & NSAIDs impair renal autoregulation so increase tendency to develop pre-renal uraemia
37
Management of pre-renal AKI
- prompt fluid replacement
38
Post- renal AKI
both urinary outflow tracts blocked | relieved if obstruction is removed
39
Renal AKI
commonly due to acute tubular necrosis --> renal ischaemia or direct renal toxins Other cuases include diseases that affect the interstitium- drug hypersensistivity infections, renal vasulature and acute glomerulonephritis)
40
Causes of acute tubular necrosis
Haemorrhage, burns, D&V, acute pancreatitis, diuretics, MI, congestive cardiac failure, endotoxic shock, snake bite, myoglobinaemia, haemoglobulinaemia, hepatorenal syndrome, radiological contrast, pre-eclapsia
41
Clinical features of AKI
- change in urine output | - biochemical abnormalities - hyperkalaemia, metabolic acidosis, hyponatraemia, hypocalcaemia& hyperphosphataemia
42
Symptoms of AKI
weakness fatigue anorexia Nausea & vomiting confusion, seziures & coma Pruritus & bruising (impaired platelet function) Breathlessness from fluid overload & anaemia
43
Management of AKI
prevention & fluid expansion
44
Chronic Kidney disease
longstanding & progressive impairment of renal function - persistent (>3/12) evidence of kidney damage ± impaired eGFR - fibrosis of remaining tubules, glomeruli & small blood vessels --> renal scarring & loss of renal function
45
Causes of CKD
DM, HTN, atherosclerotic renal vascular disease schistosomiasis (middle east)
46
Clinical features of CKD
Anaemia (increased blood loss, reduced EPO production, shortened RBC survival) Bone disease (renal phosphate retention, impaired production of Vit D 3) Neurological - polyneuropathy- peripheral paraethesiae & weakness, postural hypotension, disrupted GI motility CVD- htn, dyslipidaemia & vascular calcification
47
Goals of CKD management
- treat cause e.g. vasculitis, improve DM control - slow deterioration of renal function - Reduce CV risk - treat complications - dose adjustment for reno-toxic drugs
48
Renoprotection in CKD
BP <120/80 - ACE-i - ARB - Diuretics - CCB
49
Reducing CV risk in CKD
- optimal control of BP & reduce proteinuria - statins to lower cholesterol - cessation of smoking - optimise diabetic control - normal protein diet
50
Correction of CKD complications Hyperkalaemia
restriction of dietary potassium | stop potassium retentive drugs
51
Correction of CKD complications | calcium & phosphate
reduce dietary phosphate restriction oral phosphate binding agents (calcium carbonate) synthetic Vit D
52
Correction of CKD complications Anaemia
Can supplement with recombinant EPO
53
Correction of CKD complications Acidosis
oral sodium bicarbonate
54
Correction of CKD complications infection
increased risk of infection | vaccination - flu & pneumococcal
55
Complications of dialysis
CVD - atheroma Sepsis (peritonitis from staph aureus/ indwelling access devices) Amyloidoisis
56
Autosomal- dominant Poly cystic kidney disease (ADPKD)
cysts increase in size with age --> renal enlargement, progressive destruction of normal kidney tissue, gradual loss of renal function PKD1 gene mutation, chromosome 16
57
Clinical features of ADPKD
- acute loin pain from cyst haemorrhage/ infection/ UTI - abdominal discomfort from renal enlargement - hypertension - progressive renal impairment (end-stage renal failure in 50% pts by 50-60) - liver cyst (pancreas, spleen & ovary as well) - subarachnoid haemorrhage - mitral valve prolapse
58
Diagnosis of ADPKD
Large irregular kidneys, HTN & hepatomegaly | - definitive diagnosis on USS
59
Management of ADPKD
contro BP monitor disease progressuion (seruum creatinine) renal replacement
60
Medullary sponge kidney
uncommon condition | characterised by dilatation of collecting ducts in the papillae with cystic changes
61
Renal Cell Carcinoma | Demographics
most common renal tumour in adults present around 55 with men: women 2:1 arise from proximal tubular epithelium
62
Clinical features of renal cell carcinoma
``` Haematuria loin pain mass in the flank malaise, weight loss, fever left sided scrotal varicoceles if obstruction of gonadal vein ```
63
RCC mets
25% at presentation - bone - liver - lung
64
Management of localised RCC
radical nephrectomy | - partial if bilateral disease/ poor contralateral disease
65
Management of locally advanced/ metastatic RCC
interleukin 2 and interferon --> remission in 20% of cases | targeted immunotherapy

3B General Care (8 decks)

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