Renal Tract Flashcards
(284 cards)
1
Q
What is a urinary tract infection?
A
Infection of bladder (cystitis).
2
Q
What is the most common pathogen causing UTIs?
A
E. coli
3
Q
How does E. coli cause a UTI?
A
Transurethral ascent of colonic commensals (E. coli)
4
Q
UTIs are normally uncomplicated and resolve within a few days.
Give some risk factors for uncomplicated UTIs?
A
- Female
- Sexual activity
- Certain types of birth control; diaphragms, spermicidal agents
- Menopause
- Diabetes mellitus
5
Q
Why are females more prone to UTIs?
A
Shorter urethra
6
Q
Why can menopause predispose to UTIs?
A
Decline in circulating oestrogens in menopause causes changes in urinary tract that make you more vulnerable to infection (e.g. vaginal atrophy)
7
Q
UTIs can be complicated. Give some situations that cause a UTI to be complicated
A
- Pregnancy
- Urinary catheterisation
- Comorbidities e.g. immunosuppression
- Atypical/resistant organisms
- Structural/neurological abnormalities
- 3 months post-renal transplant
8
Q
What complication can a UTI lead to in pregnancy?
A
Pre-term delivery and low birthweight
9
Q
Give some complications of UTIs
A
- Pyelonephritis
- Urosepsis
- Impaired renal function
10
Q
What symptoms are typically seen in UTIs?
A
- Urgency
- Frequency
- Dysuria (pain)
- Suprapubic tenderness
- Foul-smelling urine
- Change in urine appearance
11
Q
In those with underlying cognitive impairment, typical features of UTIs may be absent. How may they present?
A
with delirium and reduced functional ability
12
Q
Aside from an abdo exam, what other exam may be helpful in the context of a potential UTI?
A
Genital examination if vulvovaginal atrophy or herpes simplex is possible
13
Q
What is the main sign typically seen in UTIs?
A
Suprapubic tenderness during palpation
14
Q
What is the main investigation in UTIs?
A
Urine dipstick
15
Q
What would a urine dipstick typically show in UTIs?
A
Positive for leucocytes and nitrites in most cases
16
Q
Mid stream urine samples should only be sent in which patient populations in a potential UTI?
A
- High-risk groups (e.g. pregnancy)
- Men
- Children
- Recurrent UTIs
17
Q
Typical results of a MSU in a UTI?
A
+ve for nitrites or leukocytes and RBCs → UTI likely
18
Q
If the MSU is negative for nitrites, leukocytes and RBCs in the context of a potential UTI, what does this indicate?
A
UTI less likely
19
Q
Who is a urine dipstick unreliable in?
A
- Women >65 y/o
- Catheterised patients
20
Q
What are the red flags in a UTI?
A
- Haematuria
- Loin & groin pain
- N&V
- Fever
- Rigors
- Change in mental state
21
Q
What PMH should you ensure to ask about when assessing a patient with potential UTI
A
- Possible pregnancy → get test!
- Diabetes mellitus
- Neurological conditions
- Immunosuppression
- Urolithiasis
- Bladder catheterisation
22
Q
What is the typical treatment for uncomplicated UTIs?
A
Conservative:
- Fluid intake
- Post-coital voiding
- Analgesia
23
Q
How should you safety net in the context of a UTI?
A
Any signs of fever, haematuria, loin pain, N&V, altered mental state → seek medical attention
24
Q
What is the 1st choice Abx in acute, uncomplicated UTIs?
A
Nitrofurantoin
25
What is an alternative to nitrofurantoin in UTIs?
Trimethoprim, amoxicillin, cephalexin
26
Spectrum of nitrofurantoin?
Active against most organisms that cause uncomplicated UTIs including *E. coli* (gram-negative) and *Staph. saprophyticus* (gram-positive)
27
Is E. coli gram positive or negative?
Negative
28
Mechanism of nitrofurantoin?
* Metabolised in bacterial cells by **nitrofuran reductase**
* Its active metabolite damages bacterial DNA and causes cell death (**bactericidal**)
29
Which type of bacteria are **resistant** to nitrofurantoin?
Bacteria with **lower nitrofuran reductase activity** are _resistant_ to nitrofurantoin (rare for E. coli)
30
How can nitrofurantoin affect urine colour?
Nitrofurantoin specifically can turn **urine dark yellow or brown**
31
Side effects of nitrofurantoin?
* GI upset – nausea, diarrhoea
* Immediate & delayed **hypersensitivity** reactions
* Nitrofurantoin specifically can turn **urine dark yellow or brown**
32
What side effect may occur with the use of nitrofurantoin in neonates?
haemolytic anaemia
33
Contraindications for nitrofurantoin?
* **Pregnancy** towards term (avoid in 3rd trimester)
* Babies in **first 3 months of life**
* **Renal impairment →** leads to impaired excretion, increased toxicity, and reduced efficacy
* Long term use for chronic UTIs → increases risk of adverse effects (particularly in elderly)
34
Why is nitrofurantoin contraindicated in renal impairment?
Eliminated via kidneys → leads to impaired excretion, increased toxicity, and reduced efficacy
35
How should pregnant women with **_asymptomatic bacteriuria**_ and/or _**suspected/proven UTI_** be treated?
Treat with antibiotic course (and followed up) → be careful of which trimester!!!
36
Which trimester is **trimethoprim** advised against in? Why?
1st → folate antagonist
37
Which trimester is nitrofurantoin advised against in? Why?
3rd → due to risk of haemolytic anaemia
38
Antenatal services should be informed if which pathogen is identified in the urine of a pregnant women?
group B streptococcal bacteriuria
39
What is the key differential of a UTI?
Pyelonephritis (UTI affecting the kidneys)
40
How would pyelonephritis present that could distinguish it from UTI?
Urinary symptoms +
* Febrile (pyrexia)
* Vomiting
* Loin & groin pain
* Renal angle tenderness
41
If haematuria persists following the treatment of a UTI, what may this indicate?
Possible underlying malignancy
Bladder cancer can also present with; haematuria, irritation or pain when urinating, dysuria etc
42
Mechanism of disease in pyelonephritis?
Usually bacteria travelling up from **bladder** (transurethral ascent of **colonic** **commensals**, usually E.coli)
43
Most common pathogen causes pyelonephritis?
E. coli
44
If catheter present or abnormal renal tract, what pathogen is more likely to cause pyelonephritis?
*E. coli* or *Pseudomonas aeruginosa*
45
How is a diagnosis of pyelonephritis made?
* UTI symptoms + loin pain/fever
* Culturing urinary pathogen
46
Main complication of pyelonephritis to worry about?
**Sepsis** - tachycardia, hypotension, SOB, sweating, rigors, pallor
47
Risk factors for pyelonephritis?
* Pregnancy
* Diabetes
* Structural renal abnormalities
* Immunocompromised
48
What is the key differential for pyelonephritis? How can you tell them apart?
**Cystitis →** key differential (lower UTI)
* Rarely pyrexial
* Rarely loin/flank tenderness
49
Prognosis of pyelonephritis?
* Usually responds well to antibiotic therapy – time to resolution of symptoms depends largely on **initial severity of disease** (complete and uncomplicated recovery within days to weeks).
* Prognosis less favourable in **older people** and those with **complicating factors** (e.g. immunosuppressed)
50
What important **bedside** investigations should you do in pyelonephritis?
* Urine dipstick
* Pregnancy test
51
Typical results of urine dipstick in pyelonephritis?
typically positive for leucocytes and nitrites
52
What bloods would you get in pyelonephritis?
* FBC (raised WCC)
* U&Es (check renal function)
* Blood cultures (before Abx)
53
What other test should you send to lab in pyelonephritis?
Urine MSU for MC&S → obtain sample **before** starting empirical drug treatment
54
Immediate management of pyelonephritis?
**Admit patient for IV Abx** (broad-spectrum **penicillin** with b-lactamase inhibitor/ a **cephalosporin**/a **quinolone**/**gentamicin**)
55
Which Abx are used in pyelonephritis?
Broad-spectrum **penicillin** with b-lactamase inhibitor/ a **cephalosporin**/a **quinolone**/**gentamicin**
56
Abx of choice in pregnant women with pyelonephritis?
**IV** cefalexin
57
Abx of choice in pregnant women with UTI?
**Oral** nitrofurantoin or cefalexin
58
Define urolithiasis
Renal tract calculi/renal stones/urolithiasis are hard masses that form in the urinary tract
59
Pathophysiology of renal stone formation?
Formed due to **over-saturation** of the urine
60
How can renal stone formation lead to blockage?
Stones can grow large in size, fill the hollow structures of the kidney or even travel down the ureter
Lodging of the stone in the ureter blocks the flow of urine and may result in pain.
61
What is the most common type of renal stone?
Calcium based stones (80%)
62
What are the 4 main types of renal stones?
1. Calcium based (80%)
2. Struvite (5-10%)
3. Uric acid (5-10%
4. Cysteine (1%)
63
What are struvite stones made up of?
Magnesium, ammonium & phosphate
64
There are two types of calcium based renal stones. What are they? Which is the most common?
Calcium oxalate (most common)
Calcium phosphate (less common)
65
Which type of renal stone often leads to large, staghorn calculi?
Struvite
66
Are renal stones more common in men or women?
Men
67
Are renal stones more common in older or younger generation?
Younger (\<65 y/o)
68
What & of western population do renal stones affect?
2-3% (very common)
69
What are the major predisposing factors of calcium based renal stones?
* Hypercalcaemia
* Low urine output
* High doses of vitamin D
* High purine/low Na/low K diet
70
What factors can cause hypercalcaemia that can lead to calcium based renal stones?
* Calcium supplementation
* Hyperparathyroidism
* Cancer (e.g. myeloma, breast or lung cancer)
71
What is the major predisposing factor to **struvite** renal stones?
Recurrent **_upper_** UTIs
72
Why do recurrent upper UTIs predispose to struvite stone formation?
Bacteria (UTIs) can **hydrolyse** the urea in urine to **ammonia** which can make urine more **alkaline**, leading to struvite stones
73
What is the most common organism that causes UTIs that lead to **struvite** renal stones?
**_Proteus_** infection → causes alkalinisation of the urine which leads to staghorn calculi
74
Uric acid stones often have no predisposing factors. However, which condition can increase the risk?
Gout → due to hyperuricaemia
75
What type of diet can predispose to uric acid stones?
Diet rich in purine (kidney, liver, anchovies, sardines and spinach), alcohol, gout, CKD → leads to hyperuricaemia
76
What is the major predisposing factor to cysteine renal stones?
**_Homocystinuria_** – an autosomal recessive inherited metabolic disorder which predisposes to recurrent renal stones and UTIs
77
Give some risk factors for renal stones
* Low fluid intake
* Urinary tract malformations e.g. horseshoe kidney
* UTIs
* Cystinuria (congenital)
* High sodium intake
* 1ary hyperthyroidism
* Hypervitaminosis D
* Sarcoidosis
* Cushing’s syndrome
* Milk-alkali syndrome
78
What are the 2 major complications of renal stones?
1. Obstruction → leading to AKI
2. Infection → with obstructive pyelonephritis
79
Differentials to rule out in potential renal stones (i.e. abdo pain)?
* **AAA** – rule out in men \>65 with flank pain (triad: syncope, hypotension & back pain)
* **Ectopic pregnancy** (any woman presenting with abdominal pain)
* **Pyelonephritis**
* **MSK pain**
* Shingles
* Colitis
* Bowel cancer
* Renal cancer
* Hydronephrosis
* Gallstones
80
What is the main presenting complaint in symptomatic renal stones?
Renal colic
81
Describe renal colic
* Unilateral **loin** **to** **groin** pain that can be excruciating (‘worse than childbirth) → patient can't stop moving
* **Colicky** (fluctuating in severity) as the stone moves and settles
* Caused by **increased peristalsis** around the site of obstruction
82
Give some other signs & symptoms of renal stones
* Haematuria (90% microscopic)
* N&V
* Reduced urine output
* Symptoms of sepsis if infection present e.g. fever, sweats
* Presentation of hypercalcaemia
83
Does haematuria in renal stones tend to be micro or macroscopic?
90% microscopic
84
What is the classic presentation of hypercalaemia?
‘Moans, bones, stones and groans’
## Footnote
This refers to **depressed** **mood**, **MSK** **pain**, **renal** **stones** and **abdominal** **pain**
85
What is the 1st line imaging in renal stones?
Non-contrast CT of kidneys, ureter and bladder (**CT KUB**)
86
Who should not be offered at CT KUB in renal stones? What can be offered instead?
Women \<40 y/o shouldn’t really get this 1st line due to radiation risk → offer **_US_** KUB instead
87
What bedside investigations can be performed in renal stones?
* Pregnancy test
* Urine dipstick → haematuria, possible infection
* Vital signs
* Glucose
* ECG
* Beside USS (FAST)
88
What bloods can be taken in renal stones?
* FBC – WCCs & neutrophils likely to be raised
* U&Es – creatinine & urea likely to be raised
* LFTs
* CRP
* **_Serum calcium_**
89
AXR can also be used to look at renal stones. Describe the presentation of
a) calcium based stones
b) uric acid stones
c) struvite stones
d) cysteine stones
a) smooth, opaque, silky
b) not visible (radiolucent)
c) staghorn calculus
d) yellow, semi-opaque
90
Which type of renal stone is not visible on AXR?
Uric acid (radiolucent)
91
Which type of renal stone appears yellow on AXR?
Cysteine
92
What is a staghorn calculus?
This is where the stone forms in the **shape of the renal pelvis,** giving it a similar appearance to the antlers of a deer stag (the body sits in the renal pelvis with horns extending into the renal calyces).
93
What is the management in renal stones \<5mm with no signs of obstruction?
Watchful waiting → 50-80% chance will pass spontaneously
94
What lifestyle measures should be advised in renal stones?
* Increase oral fluid intake (2-3 litres per day)
* Reduce dietary salt intake
* Maintain normal calcium intake (low dietary calcium might increase risk of stones)
95
Which drug is used in **medical expulsive therapy** in renal stones?
***tamsulosin***
96
What is 1st line analgesic in renal stones?
PR diclofenac
97
Most common surgical intervention in renal stones?
Extracorporeal shock wave lithotripsy (ESWL) → required in stones \>10mm or where there is complete obstruction/infection
98
Which drug can be offered for hypercalciuria in renal stones?
Thiazides
99
Which drug can be offered for uric acid stones?
Allopurinol or potassium citrate
100
Define hydronephrosis
**Swelling** of one or both kidneys as a result of the build-up of urine. Can also be found in unborn babies during US scans (antenatal hydronephrosis).
101
Give some risk factors for hydronephrosis
* Pregnancy
* Kidney stones
* Enlarged prostate (BPH)
* Narrowing of ureters e.g. injury, infection, surgery
* Neurogenic bladder
* Cancer
* Pelvic organ prolapse
* Vesicoureteral reflex
102
Why can pregnancy predispose to hydronephrosis?
possibly due to the **increased amount of urine** the baby produces in the **_later_** stages of pregnancy
103
Why can vesicoureteral reflux lead to hydronephrosis?
the **valve** that controls the flow of urine **between the bladder and ureters** does not function properly, allowing urine to flow **back up to the kidneys**
104
Complications of hydronephrosis?
* Can increase risk of UTIs
* In severe cases, can lead to scarring of kidneys and kidney failure
105
Prognosis of antenatal hydronephrosis?
Often resolves on its own and will cause no long-term problems for mother or baby
106
Symptoms of hydronephrosis?
* **Renal/ureteric colic:** describes an acute and severe loin pain when a urinary stones obstructs the flow of urine
* **Pain in back or sides**:
* Can be sudden and severe or a dull ache
* May be worse after drinking lots of fluids
* Symptoms of a **UTI**: frequency, dysuria, pain on urinating, fatigue, fever
* Blood in urine
* Urinating less often than you used to or with a weak stream
107
What is the diagnostic imaging investigation for hydronephrosis?
US
108
1st line management of hydronephrosis?
drain urine out of kidneys by inserting catheter
THEN treat underlying causes e.g. remove kidney stones
109
Define AKI
Defined as a rapid (within 7 days) and sustained (\>24 hours) deterioration in kidney function resulting in **oliguria** and a **rise in serum urea and creatinine**.
110
Define oliguria
\<0.5ml/kg/hour
111
Is AKI reversible?
yes
112
What classification system is used in AKI?
KDIGO
113
What is the diagnostic criteria for an AKI? (urine output, serum creatinine)
* Urine output \<0.5ml/kg/hour for 6 hours
* Serum creatinine increase 1.5x baseline over 7 days
* Serum creatinine increase by 0.3mg/dL in 48 hours
114
What 2 factors are involved in the diagnosis of AKI?
Serum creatinine & urine output
115
What defines stage 1 AKI?
Creatinine rise of **1.5x** compared to baseline or urine output \<0.5ml/kg/hour for 6 hours
116
What define stage 2 AKI?
Creatinine rise of **2x** compared to baseline or urine output \<0.5ml/kg/hour for 12 hours
117
What define stage 3 AKI?
Creatinine rise of **3x** compared to baseline or urine output \<0.3ml/kg/hour for 24 hours (or anuria for 12 hours) or serum creatinine \>354umol/dl
118
Pathophysiology behind AKI?
AKI can occur when there is a **_sudden decrease_ in glomerular filtration rate (GFR)**:
* GFR is maintained by **sufficient blood flow** into the kidneys, functioning nephrons and a clear pathway for outflow of urine from the kidney
* At the glomerular level, GFR is dependent on a **pressure gradient** between the incoming blood at the afferent capillaries and the pressure in Bowman’s space
119
Give some risk factors for AKI
* CKD
* Diabetes (with CKD)
* Heart failure
* Renal transplant
* Age \>75
* Hypovolaemia (e.g. **_sepsis_**)
* Contrast administration
* History of AKI
* Solitary kidney
* Oliguria (\<0.5ml/kg/hour)
* Liver disease
* Neurological or cognitive impairment or disability (also may mean limited access to fluids if reliance on carer)
* Drugs e.g. NSAIDs
* Symptoms or history of urological obstruction, or conditions that may lead to obstruction
120
**NSAIDs** can be implicated in multiple causes of renal impairment so their use should be restricted in patients at risk of AKI. How can they cause **pre-renal** AKI?
NSAIDs block p**rostaglandin mediated vasodilation** of the afferent arteriole, which limits the kidney’s ability to regulate local blood flow.
121
How can NSAIDs cause **intra-renal** AKI?
NSAIDs can cause acute interstitial nephritis (AIN)
122
How can NSAIDs cause **post-renal** AKI?
Long term NSAID use can cause **renal papillary necrosis** where the medullary papilla sloughs off, causing obstruction to urine flow
123
What can the causes of AKI be divided into?
1. Pre-renal
2. Intra-renal
3. Post-renal
124
How does **pre-renal** AKI occur?
Occurs when there is **reduced perfusion** to the kidney which reduces the filtration of blood.
125
Is pre, intra or post-renal AKI most common?
Pre-renal (55%)
126
What are the major causes of pre-renal AKI?
* **Dehydration**
* **Shock** - hypovolaemic, cardiogenic, distributive
* **Hypotension**
* **Renovascular disease** e.g. renal artery stenosis
* **Heart failure**
127
How does **intra-renal** AKI occur?
Occurs when there is **intrinsic disease** (structural/functional) in the kidney, leading to reduced filtration of blood.
This may occur independently or as a transformation of pre-renal AKI.
128
What are the main causes of intra-renal AKI?
* **Acute tubular necrosis (ATN)**
* **Acute interstitial nephritis (AIN)**
* **Glomerulonephritis**
* **Renal vessels -** haemolytic uraemia syndrome
129
What is the most common cause of intra-renal AKI?
Acute tubular necrosis
130
How does **post-renal** AKI occur?
Associated with **obstruction to outflow** or urine from kidney, causing back-pressure into the kidney and reduced kidney function. This is called **obstructive uropathy**.
131
What are the major causes of post-renal AKI?
Obstruction can be caused by:
* **Ureters:** nephrolithiasis (renal stones), retroperitoneal fibrosis
* **Bladder:** bladder cancer
* **Prostate:** benign prostate hyperplasia (BPH), prostate cancer
* **Urethra:** urethral stricture
* **External:** retroperitoneal mass, ovarian tumours
132
Obstruction at what level can cause a post-renal AKI in both kideys?
Obstruction at or distal to the level of the bladder can cause a **post-renal AKI in both kidneys**
Unless there is a solitary kidney, a **unilateral obstruction** may NOT cause post-renal AKI as the unaffected kidney may be able to compensate.
133
What are the major complications of AKI?
* Hyperkalaemia
* Fluid overload → pulmonary oedema, pleural effusion, peripheral oedema
* CKD
* Metabolic acidosis
* Uraemia
* Death
134
How does AKI lead to hyperkalaemia?
Injury involves the **late distal nephron** and extends into the **collecting duct**, causing direct injury of cells responsible for **K+ secretion**
135
Complications of uraemia caused by AKI?
Can lead to encephalopathy or pericarditis
136
The KDIGO system confirms an AKI with **any** of which criteria present?
* **Urine output** \<0.5ml/kg/hour for 6 hours
* **Serum creatinine** increase 1.5x baseline over 7 days
* Serum creatinine **increase** by 0.3mg/dL in 48 hours
137
Why can AKI be challenging to recognise?
AKI can be challenging to recognise as it is often **asymptomatic** or can present with **non-specific symptoms** e.g. fatigue, nausea and confusion (can often be mistaken as symptoms of the underlying condition that is causing AKI e.g. **sepsis**).
138
Give some signs seen in AKI
* Oliguria or anuria
* Signs of **hypovolaemia** → dry mucous membranes, reduced skin turgor, tachycardia, hypotension
* Signs of **volume overload** → hypertension, pulmonary oedema, peripheral oedema, elevated jugular venous pulse
* Signs of **uraemia** → uraemic encephalopathy (e.g. astrexis, confusion, seizures)
* Signs of **post-renal obstruction** → palpable or tender distended bladder (urinary retention)
139
What bedside investigations can be done in AKI?
* Vital signs
* Urinalysis
* 12-lead ECG
140
What may leucocytes and nitrites in urinalysis suggest in AKI?
infection
141
What may protein and blood in urinalysis suggest in AKI?
acute nephritis (but can be positive in infection)
142
What may glucose in urinalysis suggest in AKI?
Diabetes
143
Purpose of 12-lead ECG in AKI?
look for hyperkalaemia or pericarditis
144
What bloods would you get in AKI?
* **FBC**: anaemia, leukocytopenia, thrombocytopenia
* **_U&Es_**: creatinine, blood urea nitrogen (BUN), calcium, phosphate, potassium, sodium
* **LFTs:** serum albumin
* **VBG**: assess for acidaemia
* **ABG**: hypoxia (oedema), acidosis, potassium
145
1st line of imaging in AKI?
US kidneys ureter bladder (US KUB)
146
Why is a US KUB helpful in AKI?
* Kidney size
* Hydronephrosis
* Post-renal _obstruction_
* Renal lesions
147
Why may a CT KUB be useful in AKI?
Post-renal obstruction, renal calculi
148
Why may a CXR be useful in AKI?
pulmonary oedema
149
How you should approach an **acutely unwell** patient with suspected AKI?
DR ABCDE
150
AKI can be associated with pulmonary oedema (found in B of RRAPID). What can be given to help this?
* Sit patient up and give high flow oxygen
* Give IV **furosemide** and **diamorphine**
151
Typical ABG findings in pulmonary oedema?
Low PaO2 and low PaCO2
152
How can C be approached in AKI? (RRAPID)
Assess fluid status as patient may be hypovolaemic/hypotensive
* IV fluid resuscitation in **pre-renal** AKI
* Urine output in **post-renal** – catheterise patient where necessary
153
Give some examples of nephrotoxic drugs
NSAIDs
Antihypertensive drugs
Aminoglycosides e.g. gentamicin
Diuretics
154
Why are antihypertensives nephrotoxic?
as these reduce filtration pressure
155
What are the indications for dialysis (AEIOU)?
* **A**cidosis – severe metabolic acidosis with pH of \<7.20)
* **E**lectrolyte imbalance – persistent hyperkalaemia of \>7mM
* **I**ntoxication – poisoning
* **O**edema – refractory pulmonary oedema
* **U**raemia – encephalopathy or pericarditis
156
What type of AKI does hypovolaemia cause?
Pre-renal
157
What type of AKI does an enlarged prostate cause?
Post-renal
158
What type of AKI does a neurogenic bladder cause?
Post-renal
159
What type of AKI does heart failure cause?
Pre-renal
160
What type of AKI does sepsis cause?
Pre-renal
161
What type of AKI does acute tubular necrosis cause?
Intra-renal
162
Nephrotoxic drugs and the mechanism via which they cause renal damage
163
In the early stages of AKI, how may serum creatinine appear?
In the early stages of AKI, the reduction in GFR may coexist with a **normal serum creatinine**.
164
Define nephrotic syndrome
A clinical syndrome that arises 2ary to increased permeability of **_serum protein_** through a **damaged basement membrane** in the renal glomerulus. This leads to the **loss of significant volumes of protein** via the kidneys (proteinuria \>/=3.5g/day) which results in **hypalbuminaemia** (serum albumin =30g/L), leading to **oedema**.
165
Triad of features associated with nephrotic syndrome?
* ++ Proteinuria (\>/= 3.5g/day)
* Hypoalbuminaemia
* Oedema
166
How does nephrotic syndrome lead to **proteinuria?**
* Cytokines damage podocytes causing them to fuse together and destroy charge of the glomerular basement membrane
* This allows **increased permeability to plasma proteins** – this causes a massive protein loss in the urine
167
How does nephrotic syndrome lead to hypoalbuminaemia?
Proteinuria results in serum albumin levels being reduced beyond the synthetic ability of the liver.
168
How does nephrotic syndrome lead to oedema?
Hypoalbuminaemia results in less oncotic pressure → this lets fluid leak out into the interstitium
169
How does nephrotic syndrome lead to hyperlipidaemia?
As an attempt to **maintain oncotic pressure,** the liver tries to compensate by increased synthesis of **lipoproteins** – this is the mechanism postulated to cause the hyperlipidaemia (not fully understood)
170
How does nephrotic syndrome lead to hypercoagulability?
due to urinary losses of antithrombotic proteins and increased synthesis or prothrombotic factors)
171
What are the potential complications of nephrotic syndrome?
* **Infection** (due to urinary loss of immunoglobulins)
* **VTE** (due to urinary loss of antithrombin III)
* **Hyperlipidaemia** (due to increased hepatic production of lipids to restore the serum oncotic pressure)
172
What is the most common cause of nephrotic syndrome in adults?
**membranous glomerulonephritis**
173
What is the most common cause of nephrotic syndrome in children?
Minimal change disease
174
Other causes of nephrotic syndrome:
* **Systemic** **disease**:
* Diabetes mellitus → glomerulosclerosis
* SLE → membranous
* Amyloidosis
* **Minimal change glomerulonephritis**:
* Associated with URTI
* Treat with steroids
* **Membranous nephropathy**:
* Associated with cancers (lung, colon, breast) inflammatory conditions (SLE, thyroid), infections (hepatitis), drugs
* **Focal segmental glomerulosclerosis**:
* More common in African-Caribbean population
* Associated with Berger’s disease, sickle cell, HIV
* Biopsy – focal scarring, IgM deposition
* Treat with steroids or cyclophosphamide/ciclosporin
175
Symptoms of nephrotic syndrome?
* Triad → **proteinuria**, **hypoalbuminaemia** & **oedema**
* Peripheral oedema (more common in adults)
* Facial oedema (more common in children)
* Periorbital oedema
* Frothiness of urine (due to protein)
* Fatigue
* Recurrent infections (due to immune dysfunction)
* Venous or arterial thrombosis (e.g. myocardial infarction, DVT) due to hypercoagulability
176
Signs seen in nephrotic syndrome?
* Oedema (e.g. peri-orbital, lower limb, ascites)
* Xanthelasma and/or xanthoma (hyperlipidaemia)
* Leukonychia (hypoalbuminemia)
* SOB (with associated chest signs of pleural effusion e.g. stony dullness in lung bases) due to blood clots (hypercoagulability)
177
1st line investigation in nephrotic syndrome?
Urinalysis
178
Results of urinalysis in nephrotic syndrome?
* Proteinuria (protein +++)
* Frothy appearance
179
Describe the albumin creatinine ratio (in urine) in nephrotic syndrome
Raised albumin creatinine ratio
180
Management of nephrotic syndrome?
High dose **steroids** (tapered according to response)
181
Define nephritic syndrome
A condition involving **haematuria**, **mild to moderate proteinuria** (\<3.5g/L/day), **hypertension**, **oliguria** and **red cell casts** in the urine.
182
What is the triad of clinical features seen in nephritic syndrome?
**Haematuria**, **oliguria** & **hypertension**
183
Questions concerning nephritic syndrome often require you to distinguish between p**ost-streptococcal glomerulonephritis** and **IgA nephropathy**. What is the key distinguishing factor between the two?
**Post-streptococcal glomerulonephritis** typically presents _3-4 weeks after a sore throat infection_
**IgA nephropathy** typically presents _3-4 days after a mild URTI_.
184
Give some examples of conditions that full purely under **nephritic syndrome**
Post-streptococcal glomerulonephritis
IgA nephropathy/Henoch-Schonlein purpura
Infective endocarditis
Goodpasture’s disease
Vasculitis
185
Symptoms seen in nephritic syndrome?
* **Haematuria** (can be frank of microscopic)
* **Oedema** (to a lesser extent compared to nephrotic syndrome)
* Reduced urine output
* Uraemic symptoms (e.g. reduced appetite, fatigue, pruritis, nausea)
186
Signs seen in nephritic syndrome?
* Haematuria (visible or detectable on urinalysis)
* Oedema
* Hypertension
* Oliguria (\<300mls/day)
187
Results of urinalysis in nephritic syndrome?
* Haematuria (blood +++)
* Proteinuria (mild – protein ++)
* Red cell casts – distinguishing feature of nephritic syndrome, form in nephrons and indicate glomerular damage
188
Define CKD
A reduction in kidney function or structural damage (or both) present for **more than 3 months** (with associated health implications). CKD is classified based on the **underlying cause**, **GFR** and **proteinuria** category.
189
What is the KDIGO criteria for the presence of CKD?
* **Decreased GFR** (\<60ml/min/1.73m2) or;
* **Markers of kidney damage** (albuminuria, electrolyte abnormalities, structural or histological renal abnormalities) present for \>3 months
190
Patient is usually asymptomatic until what stage of CKD?
Stage 4/5
191
What are the 4 most common causes of CKD?
1. Diabetes
2. Hypertension
3. Chronic glomerulonephritis
4. Polycystic kidney disease
192
How can diabetes lead to CKD?
high glucose levels damages kidneys
193
How can hypertension lead to CKD?
puts strain on small vessels in kidneys
194
What infection can lead to CKD?
Streptococcal (post-strep glomerulonephritis)
195
Give some examples of nephrotoxic drugs
NSAIDs, ACE inhibitors, aminoglycosides, angiotensin II receptor antagonists, bisphosphonates, diuretics, lithium
196
The complications of CKD can be understood by considering the key functions of the kidney. What are the 5 key functions of the kidney?
1. Waste excretion
2. Fluid regulation
3. Activation of vitamin D
4. Erythropoietin production
5. Acid-base balance
197
The impairment of the kidneys ability to regulate fluid balance in CKD leads to what complications?
**Fluid overload:**
* Hypertension
* Pulmonary/peripheral oedema
198
How does CKD affect potassium levels? Why?
Causes **hyperkalaemia** → due to inability of kidneys to remove excess potassium.
199
The impairment of waste excretion in CKD leads to what 2 major complications?
* **Uraemia** (as uric acid is filtered through the kidney) → gout?
* **Hyperphosphataemia** (phosphates are waste products of metabolism)
200
How does CKD affect the acid-base balance?
**Metabolic acidosi**s due to:
* impaired **ammonia** **excretion**
* reduced tubular **bicarbonate** **reabsorption**
* insufficient renal **bicarbonate** **production**
201
Why can CKD lead to anaemia?
Kidneys responsible for EPO production
202
How does CKD affect calcium levels? Why?
**Hypocalcaemia** due to 2 mechanisms::
1. **Phosphate** not removed from blood, causing hypocalcaemia in blood as more calcium binds to the excess phosphate
2. **Vitamin D** is no longer converted to its active form by the kidneys, causing **inadequate calcium absorption** from the gut → levels of calcium in the blood falls, triggering the release of PTH
203
How does CKD affect **parathyroid** hormone levels? Why?
Levels of calcium in the blood falls, triggering the release of PTH → hypocalcaemia can trigger 2ary **hyperparathyroidism**
204
Complications can be remembered by the pneumonic CRF HEALS. What are these?
* **C** - Cardiovascular disease
* **R** - Renal osteodystrophy
* **F** - Fluid (oedema)
* **H** - Hypertension
* **E** - Electrolyte disturbance (hyperkalaemia, acidosis)
* **A** - Anaemia
* **L** - Leg restlessness
* **S** - Sensory neuropathy
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Why can CKD cause restless legs?
* Anaemia and/or
* Iron deficiency and/or
* Hypocalcaemia
206
What is the most common cause of death in CKD?
CVS disease
207
What is renal osteodystrophy? Why is it seen in CKD?
Caused by disturbed vitamin D, calcium, PTH and phosphate metabolism causing **abnormalities in bone turnover and mineralisation**
Features:
* Reduced bone density (osteoporosis)
* Reduced bone mineralisation (osteomalacia)
* 2ary/3ary hyperparathyroidism
* May get spinal osteosclerosis
208
Which 2 factors can be used as prognostic indicators in CKD?
* Increasing proteinuria and/or
* Decreasing eGFR
209
Potential signs of CKD?
* **Oedema**
* **Pallor** (due to renal anaemia)
* **Cachexia**, signs of malnutrition
* **Frothy urine** (proteinuria)
* **Cognitive impairment** (language, orientation, attention)
* **Tachypnoea** (fluid overload, anaemia, co-morbid ischaemic heart disease)
* **Palpable distended bladder** (obstructive uropathy)
210
What is a albumin:creatinine ratio?
Also known as **microalbumin.**
Involves measuring the amount of albumin in the urine. The amount of urine albumin is compared with the quantity of creatinine (waste product in urine).
211
what does a high urine albumin creatinine ratio mean?
kidney disease → poor prognostic indicator
212
What bloods should be done in CKD?
* FBC → anaemia?
* U&Es
* eGFR
* Serum creatinine
* Serum calcium → low?
* Serum phosphate → raised?
* PTH tests
213
What urine tests should be done in CKD?
* Early morning urine sample → urinary albumin:creatinine ratio (ACR)
* Urine dipstick → haematuria
214
How can **anaemia** in CKD be managed?
Monthly **subcutaneous erythropoietin injections** (target Hb 10-12 g/dL)
NOTE → This should **NOT** be given in the context of iron deficiency anaemia as can worsen symptoms (check ferritin levels)
215
How common is BPH?
**BPH is the most common prostate problem in men**. Almost all men will develop some enlargement of the prostate as they grow older. By age 60, 50% of men will have some signs of BPH; by age 85, 90% of men will have signs of the condition.
216
Risk factors for BPH?
* Men \>50 y/o (hormonal changes):
* Family history
* Diabetes and heart disease (as well as use of beta blockers)
* Lifestyle – obesity increases risk
217
Effect of BPH on prostate cancer risk?
**NO increased risk of developing prostate cancer!**
218
Potential complications of BPH?
* Urinary symptoms (LUTS)
* Bladder, urinary tract or kidney damage
* Urinary retention
* UTIs
* Bladder stones
* Bladder damage
219
What is the **key symptom** in BPH?
Lower urinary tract symptoms (LUTS)
220
What are LUTS?
These can be:
a) storage symptoms
b) voiding symptoms
c) post-micturition symptoms
221
Give some examples of **storage** LUTS
urgency, daytime urinary frequency, nocturia, urinary incontinence
222
Give some examples of **voiding** LUTS
weak urine stream or stream that stops at starts, difficulty starting urination
223
Give some examples of post-micturition LUTS
dribbling at end of urination, inability to completely empty bladder
224
What should be ruled out in those presenting with possible BPH?
Urinary retention
225
Investigations in BPH?
* DRE to assess prostate for size, constituency, nodules and tenderness → should reveal **benign-feeling, enlarged prostate with no obvious nodules**
* Urine dipstick for blood, glucose, protein, leucocytes, nitrites → can rule out infection or other conditions
* Serum creatinine & eGFR → can indicate kidney problems
* PSA testing → prostate cancer ??
226
Lifestyle changes in BPH?
* Less alcohol, caffeine, fizzy drinks
* Exercise
* Limit artificial sweeteners
* Drink less fluids in evening
227
What is the 1st line pharmacological treatment in BPH?
Alpha blockers (Doxazosin, Tamsulosin)
228
What is the 2nd line pharmacological treatment in BPH?
5a-reductase inhibitors (e.g. finasteride)
229
Mechanism of alpha blockers vs 5a-reductase inhibitors in BPH?
Alpha blockers → relax bladder neck muscles and muscle fibres in prostate, making urination easier
5a-reductase inhibitors → shrink prostate by preventing hormonal changes
230
What hormone is prostate cancer almost always reliant on?
Testosterone
231
What is the most common type of prostate carcinoma?
Adenocarcinoma
232
Most common zone that prostate carcinoma is found in?
Peripheral zone
233
Risk factors for prostate cancer?
* Increasing age
* FH
* BRCA mutation
* Black African or Caribbean origin
* Tall stature
* Anabolic steroids
* Obesity
* Smoking
* Diet (high in animal fats and milk products)
234
Symptoms/signs in prostate cancer?
* Lower urinary tract symptoms (LUTS) – similar to BPH
* Haematuria
* Erectile dysfunction
* Discomfort in pelvic area
* Symptoms of advanced disease or metastasis:
* Weight loss
* Cauda equina syndrome
* Bone pain
235
What are the 2 1st line investigations in suspected prostate carcinoma?
* PR exam
* Urine dip
236
What may a cancerous prostate feel like on a PR exam?
firm or hard, craggy, or irregular, with loss of central sulcus, may be a hard nodule → **2 week wait urgent cancer referral to urology**
237
What blood test can be done in prostate cancer? What are the issues with it?
PSA (prostate specific antigen) → Counselling prior due to poor sensitivity and specificity
238
1st lin imaging in prostate cancer?
MRI
239
What scale is used to interpret MRI results of prostate cancer and guide next investigations?
Likert scale
240
What Likert scale result warrant a prostate biopsy?
Likert 3 or above
241
What grading system is used for prostate cancer?
Gleason scale
242
How is the Gleason score calculated?
The Gleason score is made up for **two numbers** added together for the total score (e.g. 3 + 4 = 7):
* 1st number → grade of most prevalent pattern in biopsy
* 2nd number → grade of 2nd most prevalent pattern in biopsy
243
Describe 1-5 of the Gleason Score
* 1 – Normal tissue, well differentiated cells that are small and uniform
* 2 – Increased stroma between glands
* 3 – Distinctly infiltrative margins, moderately differentiated cells
* 4 – Irregular masses of neoplastic glands, poorly differentiated
* 5 – Occasional gland formation seen, very poorly differentiated
244
What **staging** system is used in prostate cancer?
TNM:
* TX – unable to assess size
* T1 – too small to be felt on examination or seen on scans
* T2 – contained within prostate
* T3 – extends out of prostate
* T4 – spread to nearby organs
Nodes:
* NX – unable to assess nodes
* N0 – no nodal spread
* N1 – spread to lymph nodes
Metastasis:
* M0 – no metastasis
* M1 – metastasis
245
Main non-hormonal option in the treatment of prostate cancer?
**External beam radiotherapy** directed at prostate
246
What is the 1st line **hormonal** option in the management of prostate cancer?
GnRH analogues/agonists (e.g. *Goserelin, Leuprolide)*
247
What class of drugs are *Goserelin, Leuprolide*?
GnRH analogues/agonists
248
GnRH agonists can cause a transient rise in testosterone. What drug can be given to counteract this?
Androgen antagonists/anti-androgens (bicalutamide, enzalutamie).
These drugs prevent an increase in disease activity following a transient surge in LH & FSH.
249
Side effects of hormonal treatment in prostate cancer?
* Decreased libido
* Impotence
* Infertility
* Gynecomastia
* Weight gain
* Osteoporosis
* Diabetes
* IHD
* Anaemia
250
What is PSA produced by?
The **epithelial cells** of the prostate produce PSA.
251
What is PSA?
PSA is a **glycoprotein** that is secreted in the semen, with a very small amount entering the blood.
252
Function of PSA?
Its **enzymatic activity** helps **thin** the thick semen into a liquid consistency after ejaculation.
253
Rate of false positives and false negatives in PSA testing?
PSA testing is **unreliable** with a high rate of **false positives** (75%) and **false negatives** (15%)
254
Some common causes of a raised PSA?
* Prostate cancer
* Acute urinary retention
* BPH
* Recent ejaculation or prostate stimulation
* PR exam
* UTI
* Prostatitis
* Prostate cancer
* Urethral instrumentation
* Vigorous exercise (notably cycling)
If any of these are present, it would be wise to avoid a PSA test as it would raise the possibility of investigation.
255
Define hyperkalaemia
Plasma potassium in excess of \>/= 5.5 mmol/L
* Mild → 5.5-5.9 mmol/L
* Moderate → 6.0-6.4 mmol/L
* Severe → \>6.5 mmol/L
256
What is the most common cause of hyperkalaemia?
Kidney disease:
* AKI
* CKD
* Hyperkalaemic renal tubular acidosis
257
Why are the kidneys the most common cause of hyperkalaemia?
Kidneys are responsible for 90% of potassium excretion, with the rest being excreted via the GI tract.
258
Which medications can result in hyperkalaemia?
* ACEi
* ARBs
* Potassium-sparing diuretics
* NSAIDs/COX2 inhibitors
* Digoxin (in toxicity)
* Trimethoprim
* Beta blockers – selective and non-selective
* Nicorandil
* Heparin – UH and LMWH
* Ciclosporin
* Tacrolimus
* Renin-inhibitors (e.g. aliskiren)
* Potassium supplements
* **IV fluids** **containing potassium** when used inappropriately
259
How can trauma/burns affect potassium?
Tissue damage 2ary to trauma or burns results in the release of significant volumes of potassium from damaged cells
260
How can DKA affect potassium levels?
In DKA, potassium shifts from **intracellular to extracellular space** due to **lack of insulin**, resulting in _hyperkalaemia_
261
How does aldosterone affect potassium?
Aldosterone promotes excretion of potassium by the kidneys
262
How does Addison's disease affect potassium levels?
* Aldosterone promotes excretion of potassium by the kidneys
* In Addison’s disease, the adrenal glands are unable to produce adequate levels of **aldosterone** which results in **reduced renal excretion of potassium**
* Aldosterone causes sodium to be absorbed and potassium to be excreted
263
ECG signs of hyperkalaemia?
* Tall tented T waves
* Wide QRS complexes
* Prolonged PR interval
* Flattened P waves
* AV block
264
Why can hyperkalaemia lead to bradycardia?
Due to hyperkalaemia-induced AV block
265
Bedside tests to do in hyperkalaemia?
* Vital signs
* 12 lead ECG
* Capillary blood glucose → rule out hyperglycaemia (e.g. DKA)
266
Bloods to do in hyperkalaemia?
* FBC
* U&Es
* Confirm presence of hyperkalaemia and assess other electrolytes
* Assess renal function (kidneys responsible for 90% of potassium excretion)
* **ABG** → rule out metabolic acidosis (e.g. hyperkalaemic renal tubular acidosis or DKA)
* **Serum cortisol →** rule out Addison’s disease (low serum cortisol)
* **Digoxin level** → rule out toxicity (if relevant)
267
What is management of hyperkalaemia determined by?
the **level of potassium** and the **presence/absence of associated ECG changes**
268
What is the pharmacological management of hyperkalaemia if there are **hyperkalaemia associated ECG changes** present?
IV calcium gluconate
269
Purpose of calcium gluconate in hyperkalaemia?
Should help stabilise the myocardium temporarily for 30-60 minutes and reduce risk of fatal arrhythmia
270
What 2 pharmacological agents can be used in hyperkalaemia to help **shift potassium intracellularly?**
1. Insulin-glucose infusion
2. Salbutamol
271
How can salbutamol help in hyperkalaemia?
Often used as adjuvant therapy for hyperkalaemia as it promotes the movement of potassium into cells and out of serum
272
How can insulin-glucose infusion help in hyperkalaemia?
* **Insulin** helps to shift potassium from the extracellular to intracellular compartment
* **Glucose** helps to maintain capillary blood glucose levels
273
Mechanism of c**alcium polystyrene sulfonate resin (Calcium resonium)** in hyperkalaemia?
Can be used to remove potassium via the GI tract
274
What is the most common type of bladder carcinoma?
**Transitional Cell Carcinoma**
275
Risk factors for transitional cell carcinoma (bladder)?
* Smoking
* Aromatic amines (rubber, dyes, chemical industry)
* Cyclophosphamide
276
Risk factors for squamous cell carcinoma (bladder)?
* Schistosomiasis infection
* Long term catheterisation (10+ years)
277
What type of bladder cancer can schistosomiasis infection predispose you to?
Squamous cell carcinoma
278
What symptoms is considered **bladder cancer** until proven otherwise?
Painless haematuria (visible)
279
What is the most common type of **renal** carcinoma?
Adenocarcinoma
280
Which 3 cancers most commonly cause hypercalcaemia?
1. Breast
2. Lung
3. Myeloma
281
What triad of symptoms does an AAA present with?
Syncope, hypotension and back pain
282
What is haemolytic uraemic syndrome?
A condition that can occur when the **small** **blood vessels** in your kidneys become **damaged** and **inflamed**. This damage can cause **_clots_** to form in the vessels. The clots clog the filtering system in the kidneys and lead to **kidney** **failure.** Can result in:
* the destruction of blood platelets (cells involved in clotting)
* a low red blood cell count (anemia)
* kidney failure due to damage to the tiny blood vessels of the kidneys
283
Give 3 classes of medications used in the management of prostate cancer
1. GnRH analogues (e.g. Goserelin)
2. GnRH antagonists (e.g. Degarelix)
3. Androgen antagonists (e.g. Bicalutamide, Enzalutamide)
284
What is the key Abx that causes hyperkalaemia?
Trimethorprim
