Brainscape's Knowledge GenomeTM

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


See full index

Year 3 Medicine > Renal > Flashcards

Renal Flashcards

1
Q

What is the normal anion gap?

A

10-18 mmol/l

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

Give 3 symptoms of HYPERnatraemia

A

Thirst
Irritability
Weakness

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

Give two causes of HYPOvolaemic HYPERnatraemia

A

Loop Diuresis (Renal Loss)
Burns (Non Renal Loss)

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

Give two causes of EUvolaemic HYPERnatraemia

A

Diabetes Insipidus
Hypodipsia

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

Give two causes of HYPERvolaemic HYPERnatraemia

A

Hypertonic Dialysis
Cushings

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

What is the triad of Diabetes Insipidus?

A

Polydipsia, Polyuria, Dilute Urine

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

Give two causes of Central DI

A

TB
Sarcoidosis

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

Give two causes of Nephrogenic DI

A

Congenital
Drugs (Lithium, Amphoterecin, Demeclocycline)

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

What three investigation results would prove DI

A

Serum Osmolality>295
Urine Osmolality<300
Water Deprivation test - low urine osmolality before and after, cranial or nephrogenic depends on desmopressin response

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

Using the mnemonic SALT LOSS, what are the features of HYPOnatraemia?

A

Stupor, Anorexia, Lethargy, Tendon reflexes decreased, Limp muscles, Orthostatic hypotension, Seizures, Stomach cramping

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

What are two causes of HYPOvolaemic HYPOnatraemia? How would you differentiate between them?

A

Addisons (renal)
Burns (non renal)
Differentiated by urinary sodium

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

What are two causes of EUvolaemic HYPOnatraemia?

A

Primary Polydipsia
SIADH
Differentiated by urinary concentration

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

What are two causes of HYPERvolaemic HYPOnatraemia

A

CCF
Liver Failure

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

Name three drugs you could use to treat SIADH (by inducing DI)?

A

Lithium
Amphoterecin
Demeclocycline

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

How would you treat HYPER and HYPOvolaemic HYPOnatraemia respectively?

A

HYPO- IV 0.9% saline
HYPER - Fluid restrict and consider furosemide

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

Give 4 causes of HYPERkalaemia

A

CKD
Rhabdomyolysis
Addisons
Drugs

Emergency if K+>6.5mmol/l
OR
K+>5.3mmol/l with ECG changes

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

Using the mnemonic THANKS CYCLE, what drugs contribute to HYPERkalaemia?

A

Trimethoprim
Heparin
ACEI
NSAIDs
K+ Sparing DIuretics
Succinyl Choline
Cyclosporine

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

What is Type 4 RTA?

A

Occurs when there is low aldosterone activity
May be Hyperkalaemic, Hyperchloraemic

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

Give 4 possible ECG changes for HYPERkalaemia

A

WAFT

Widened QRS
Asystole
Flattened P
Tented T

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

What are three possible presentations of HYPERkalaemia?

A

Fatigue
Paraesthesia
Chest Pain

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

Give a four step management plan for HYPERkalaemia

A

Manage if levels >6.5 or ECG changes

1) 10mls 10% Calcium Gluconate over 10 mins
2) Actrapid+IV dextrose/glucose solution
3) Nebulised Salbutamol
4) Calcium Resonium

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

What are three possible presentations of HYPOkalaemia?

A

Fatigue
Constipation
Proximal Muscle Weakness

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

Give three drugs which could cause HYPOkalaemia

A

Doxazosin
Salbutamol
Insulin

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

Apart from drugs and N and V, give 3 other causes of HYPOkalaemia

A

Refeeding Syndrome
Conns Syndrome
Liquorice

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

Give 3 ECG changes of HYPOkalaemia

A

Low T waves
High U waves
Prolonged PR interval

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

Apart from replacing Potassium in HYPOkalaemia, what other electrolyte would you consider replacing?

A

Magnesium

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

Define AKI

A

Reduced renal function occurring over hours to days
A rise in creatinine more than 50% in the last 7 days

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

Give two causes of PRE RENAL AKI

A

Hypovolaemia
Renal Artery Stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Give a tubular, glomerular and vascular cause of INTRARENAL AKI

A

Glomerular - Acute Glomerulonephritis
Tubular - Acute tubular necrosis (endo - myoglobin, exo - contrast)
Vascular - Vasculitis

Acute interstitial neohritis

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

Give two causes of POSTRENAL AKI

A

BPH
Bladder Outflow Obstruction

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

If you thought the AKI might be due due to Post Streptococcal Glomerulonephritis, what investigation would you do?

A

Anti Streptolysins Titre

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

Name 4 Investigations for AKI

A

Urine Dipstick
Daily Bloods (Inc CK- Rhabdomyolysis, LFTs - Hepatorenal), VBG
Urine PCR, M, C, S
USS KUB

?post-void bladder scan

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

How do you calculate IV flow rate?

A

IV Flow Rate = (drop factor * vol)/time

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

What Nephrotoxic agents should you discontinue in an AKI? Give 4

A

Aminoglycosides
Vancomycin
Acyclovir
NSAIDs

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

Give 3 indications for Renal Replacement Therapy in an AKI

A

Refractory Hyperkalaemia
Uraemic Encephalopathy
Uraemic Pericarditis

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

What are the four characteristics of Nephrotic Syndrome?

A

Oedema
Proteinuria (>3.5g in 24 hours) (Frothy Urine)
Hypoalbuminaemia (<30)
Hypercholesterolaemia

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

Give the four main causes of Nephrotic Syndrome

A

Minimal Change Disease
Membranous Nephropathy
Focal Segmental GlomeruloSclerosis
Diabetes

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

Give the four main presenting features of Nephritic Syndrome

A

Haematuria
Hypertension
Hardly any urine
Proteinuria

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

Describe the pathophysiology of Post Streptococcal GN

A

Occurs weeks after Group A/B Strep Infection
1-2 weeks post tonsillitis
3-4 weeks post impetigo/cellulitis
Normally affects children aged 3-12

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

What would a serum sample of Post Streptococcal GN show?

A

Low C3
Anti Strep Antibodies

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

How would you manage Post Streptococcal GN?

A

Self Limiting
ACEI/ARB for proteinuria

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

Describe the pathophysiology of IgA Nephropathy

A

Haematuria after an URTI, GI Infection
Peak incidence in 20-30 y/o

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

Describe the findings in a serum/urine/biopsy of IgA Nephropathy

A

Serum - High IgA, Normal C3/C4
Urine - Asymptomatic microhaematuria with intermittent visible
Biopsy - Mesangial Immune Complexes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

State the three different types of ANCA/Small Vessel Vasculitis

A

Granulomatosis with Polyangitis
Microscopic Polangitis
Churg Strauss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Describe the features of Granulomatosis with Polyangitis

A

C-ANCA
Pulmonary and Nasopharyngeal involvement (haemoptysis and nasal polyps)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Describe the features of Microscopic Polyangitis

A

P-ANCA
Mild Respiratory Symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Describe the features of Churg Strauss

A

P-ANCA
Asthma, Allergic Rhinitis, Peripheral Neuropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Describe the pathophysiology of Anti GBM disease

A

Antibodies against type 4 collagen
Type 4 collagen also lies in Respiratory System therefore haemoptysis

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

What would serum sample/CXR/biopsy of Anti GBM show?

A

Serum - Anti GBM Antibodies
CXR - Pulmonary Infiltrates
Biopsy - Deposition of IgG along basement membrane

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

How would you treat Anti GBM disease?

A

Plasma Exchange and Immunosupression

51
Q

Describe the pathophysiology of Thin Basement Membrane Disease

A

Hereditary Abnormalities of Type 4 collagen cauisng microscopic haematuria
Biopsy shows diffuse thinning of GBM

52
Q

What is Alport Syndrome?

A

X linked abnormalities in Type 4 collagen, also causing hearing loss and eye abnormalities

53
Q

How does the biopsy of Alport and Thin Basement Membrane disease differ

A

Thin Basement Membrane - Diffuse thinning
Alport - Alternate thinning and thickening

54
Q

Why should you give LMWH prophylactically in Nephrotic Syndrome?

A

Low albumin increases VTE risk
It is an acute phase reactant normally with anticoag properties

55
Q

Define CKD

A

Presence of kidney damage with abnormal albumin excretion/decreased function, persisting more than 3 months

56
Q

Describe the classifications of CKD in term of GFR, from G1-G5

A

G1 - >90
G2 - 60-89
G3a - 45-59
G3b - 30 - 44
G4 - 15-29
G5 - <15

57
Q

How could you classify the Albumin Creatinine Ratio in CKD?

A

A1 - <3
A2 - 3-30
A3 - >30

58
Q

What drug could cause hypertrophy of the gums? What would this indicate?

A

Cyclosporin
Renal Transplant

59
Q

Give four complications of CKD

A

Anaemia of Chronic Disease
Mineral Bone Disease
Hyperparathyroidism
Hypertension

60
Q

What is the link between Hypertension and CKD?

A

Chronic raised BP causes Nephrosclerosis
Renal Artery Stenosis causes Hypertension (investigate with Magnetic Resonant Angiogram)

61
Q

Describe the genetics of APCKD

A

Autosomal Dominant
Type 1 (85%) - Mutation on Chromosome 16
Type 2 (15%) - Mutation on Chromosome 4, slower course, reaches end stage renal failure sooner

62
Q

Give 4 clinical presentations of APCKD

A

Loin Pain
Visible Haematuria
Renal Calculi
High BP

63
Q

Name three disease associations of APCKD

A

Mitral Valve Prolapse
Ovarian Cysts
SAH

64
Q

How would you diagnose ADPCKD?

A

Family History and USS (although cysts aren’t usually visible until after the age of 30)

65
Q

How would you treat APCKD?

A

Controlling BP (NOT with CCB though)
Tolvaptan (ADH antagonist) may slow growth

66
Q

Describe four reasons why someone may have Anaemia of Chronic Disease in CKD

A

Reduced Erythropoietin production
Absolute Iron Deficiency (Malnutrition)
Functional Iron Deficiency (Inflammation)
Bone Marrow Supression from Uraemia

67
Q

How would you manage ACD in CKD?

A

Replace any Haematinics that need replacing
Give ESA (Erythropoietin Stimulating Agent)

68
Q

Give two causes of CKD Mineral Bone Disease with LOW turnover

A

Osteomalacia (Vit D Deficiency)
Adynamic Bone Disease (low osteoclasts and osteoblasts)

69
Q

Give one cause of CKD Mineral Bone Disease with HIGH turnover

A

Osteitis FIbrosa (complication of hyperparathyroidism - soft areas of bone with no calcium)

70
Q

Give a brief description of Vit D Metabolism

A

Cholecalciferol is converted to calcidiol in the liver
Calcidiol is converted to Calcitriol by 1a Hydroxylase in Kidneys
1a Hydroxylase is upregulated by PTH

71
Q

What is Tertiary Hyperparathyroidism?

A

Persistent high PTH despite high calcium

72
Q

Give two advantage and two disadvantages to Peritoneal Dialysis

A

Advantages - Good QoL, More individualised
Disadvantages - Risk of Infection, Unsuitable for previous abdo surgeries

73
Q

Give three complications of Peritoneal Dialysis

A

Peritonitis
Hernia
Leak

74
Q

What are the three subtypes of Peritoneal Dialysis?

A

Automated - overnight exchange 10-12L over 8-10 hours leaving daytime free
Continuous Ambulatory - 4-5 exchanges throughout the day at regular intervals
Assisted Automated

75
Q

Give 4 disadvantages of Haemodialysis

A

Bacteraemia
Haemodynamic Instability
Cramps
SVCO

76
Q

What is AV Fistula Steal Syndrome?

A

Reduced oxygenation of tissue distal to the fistula due ot mixing of oxygenated and deoxygenated blood

77
Q

What is Active Conservative Management, and who recieves it?

A

When Renal Replacement Therapy offers no survival benefit
If over 80 or if WHO Performance Score>3

78
Q

When is Renal Transplant contraindicated?

A

Active infection/malignancy
Severe heart/lung disease
Uncontrolled substance abuse
Psychiatric Illness

79
Q

Living related donor is the best option for transplant, what are the four types of Living UNrelated donor?

A

Living Donor Paired Exchange
Living Donor Deceased Exchange
Live Donor Chain
Altruisic Donation (donated into pool)

80
Q

What is the Induction treatment for a Kidney Transplant?

A

Methylprednisolone usually in combination with Rituximab

81
Q

What is the Maintenance treatment for a Kidney Transplant?

A

Prednisolone
Calcineurin Inhibitors - Tacrolimus/Cyclosporine
Rapamycin Inhibitors - Everolimus

82
Q

What is Polyomavirus?

A

Childhood infection of flu like symptoms which stay latent forever
Can become reactivated post transplant, causing renal infection and rejection
Look out for changes in vision/urination

83
Q

What is Myeloma?

A

Abnormal proliferation of single clone of Plasma Cells leading to secretion of Immunoglobulins

84
Q

Give 3 systemic complications of Myeloma

A

Osteolytic Bone Lesions (Backache)
Hypercalcaemia (myeloma cells increase signalling of osteoclasts)
Recurrent bacterial infection

85
Q

How does Myeloma affect the Kidneys?

A

Deposition of IgG/Light Chains in glomerulus causing Tubular Obsttruction/Proteinuria

86
Q

What is Radiocontrast Nephropathy and how can you prevent it?

A

AKI 48-72 hours after IV contrast
Prevented with pre hydration with IV Crystalloid and the discontinuation of Nephrotoxic drugs 24h pre and post procedure

87
Q

What is Urate Nephropathy?

A

Uric acid crystals precipitate in the tubule interstitium
Decreases GFR and causes inflammation

88
Q

How would Urate Nephropathy present?

A

Mild Proteinuria
Slight increase in serum creatinine

89
Q

How would you manage Urate Nephropathy?

A

Tumour Lysis - Excessive Hydration
Allopurinol/Febuxostat

90
Q

What is a Phakomatose?

A

Neurocutaneous syndromes arising from embryonic ectoderm causing systemic hamartomas
An example is Tuberous Sclerosis - can cause Renal Angiomyolipomas

91
Q

Name the two types of Phakomatoses affecting the Kidney

A

Tuberous Sclerosis Complex (Pringle’s Disease)
Vin Hippel Lindau Syndrome

92
Q

What is the main complication of Von Hippel Lindau Syndrome?

A

Renal Cysts and Clear Cell Renal Carcinoma by the age of 40

93
Q

What are the three types of Membranoproliferative Syndrome? How would it appear microscopically?

A

Type 1 - Hep C
Type 2 - Caused by persistent activation of compliment pathway, low circulating levels of C3
Type 3 - Hep B and Hep C
‘Tram Tracks’

94
Q

What are the two types of Nodular Glomeulonephritis? How would you differentiate between them?

A

Diabetic and Amyloid Nephropathy
Diabetic - Congo red negative
Amyloid - Congo positive and apple green bifringence

95
Q

Name 3 ANCA -ve small vessel vasculitis

A

HSP (Henoch-Schonlein purpura)
Behcets
Goodpastures

96
Q

What glomerulonephropathies will ONLY present as crescenteric/RPGN?

A

ANCA +ve
Goodpastures

97
Q

If the cause of the nephropathy is Drug Induced Lupus, what is the drug?

A

TNF Inhibitor such as Infliximab

98
Q

It can be hard to differentiate between Post IgA nephropathy and Post Strep Nephropathy, what is the difference in timescales of renal manifestations?

A

IgA = 2-3 days
Strep = 2-3 weeks

99
Q

Give 3 causes of Membranous Nephropathy

A

Lupus
Malignancy (Lung, Colon, Haematological)
Hep B/C

100
Q

Give two secondary causes of FSGS

A

Heroin
HIV

101
Q

Describe the stages of AKI in terms of Serum Creatinine

A

Stage 1: 1.5-1.9 x baseline
Stage 2: 2-2.9 x baseline
Stage 3: 3 x baseline

102
Q

Describe the stages of AKI in terms of Urine Output

A

Stage 1: <0.5ml/kg/h for 6-12hrs
Stage 2: <0.5ml/kg/h for atleast 12hrs
Stage 3: <0.3ml/kg/h for atleast 24hrs

103
Q

Using the STOP mnemonic, how would you acutely manage an AKI?

A

Sepsis - Appropriate Abx
Toxins - Stop any nephrotoxic medications
Optimising Fluids - Likely to be dehydrated
Prevent Harm

104
Q

Name five drugs that are safe to continue in an AKI

A

Paracetamol, Warfarin, Statins, Beta Agonists, Asparin

105
Q

Name 4 types of renal stones and state the most common

A

Calcium Oxalate (most common)
Cystine
Urate
Calcium Phosphate
Struvite (ammonia, phosphate and magnesium)

106
Q

Which stone is radiolucent?

(IE won’t show up on radiology)

A

Urate

107
Q

Give three general risk factors for renal stones

A

Dehydration
Horseshoe kidney
Disorders of metabolism

108
Q

Name three associations of urate stones

A

Gout
Ileostomy (reduces bicarbonate)
Malignancy

109
Q

Name three drugs that increase calcium oxalate stones and one that decreases

A

Increases : Steroids, Loop diuretics, Acetazolamide

Decreases : Thiazide

110
Q

How are suspected renal calculus investigated?

A

1) Urinalysis and culture
2) Bloods (inc U and Es, and clotting if percutaneous intervention)
3) Non Contrast CTKUB - urgency depends on presentation (USS if pregnant)

111
Q

Describe the management of renal calculi

A

Initial IM/PR Diclofenac

<5mm in ureter - conservative (+/- tamsulosin)
>2mm in renal pelvis - ESWL
Infection - Urgent nephrostomy
Stag horn - Nephrolithotomy
Pregnancy - Uteroscopy

112
Q

What should you do after resolution of renal calculi?

A

Consider underlying cause

113
Q

What is Renal Artery Stenosis? State the two most common causes

A

Narrowing of the afferent arteriole

Atherosclerosis
Fibromuscular Dysplasia (beads on a string)

114
Q

Describe the pathophysiology associated with Renal Artery Stenosis

A

Blood flow -> afferent arteriole-glomerulus-efferent arteriole-vasa recta- venous outflow

Cells in the DCT (macula densa) release PGs as they sense low sodium from filtrate
Causes juxtaglomerular cells in afferent arteriole to release renin
Increasing BP but glomerular flow remains low - atrophy

115
Q

What might you hear O/E renal artery stenosis?

A

Renal artery bruits

116
Q

How would you investigate renal artery stenosis?

A

1) Urinalysis
2) FBC , U and Es
3) USS, CT Angio

117
Q

How is renal artery stenosis managed?

A

Control of BP

Stent/Angioplasty/Bypass

Kidney removal

118
Q

How would you investigate nephrotic syndrome?

A

Urinalysis
24h Urine Protein
Albumin:Creatinine ratio
Serum albumin

119
Q

What is Acute Tubular Necrosis

A

Most common cause of AKI

Ischaemia and necrosis of epithelial tubule cells due to either reduced perfusion of rhabdomyolysis/NSAIDs/contrast dye

120
Q

What is characteristic of acute tubular necrosis?

A

Brown muddy casts

121
Q

How can Acute tubular necrosis be differentiated from pre renal AKI?

A

More dilute urine

122
Q

What is Acute Interstitial Nephritis?

A

Hypersensitivity reaction

Typically due to NSAIDS/Abx

Presents as rash/fever/eosinophilia

123
Q

Name two distinguishing features between AKI and CKD

A

AKI - normal size kidneys, Hyperkalaemia

CKD - small kidneys, hypocalcaemia

Year 3 Medicine (10 decks)

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