Urology and renal Flashcards
1
Q
what is Lymphogranuloma venereum (LGV) caused by
A
Chlamydia trachomatis serovars L1, L2 and L3
2
Q
Risk factors for Lymphogranuloma venereum (LGV)
A
Men who have sex with men
majority of patients who present in developed countries have HIV
historically was seen more in the tropics
3
Q
three stages of Lymphogranuloma venereum (LGV)
A
1: small painless pustule which later forms an ulcer
2: painful inguinal lymphadenopathy (may occasionally form fistulating buboes)
3: proctolitis
4
Q
How is Lymphogranuloma venereum (LGV) treated
A
doxycycline
5
Q
Indication for dialysis in aspirin overdose
A
acute renal failure
pulmonary oedema
metabolic acidosis resistant to treatment
seizures
comas
serum concentration of salicylic acid >700mg/L
6
Q
Key concept for Salicylate overdose
A
leads to mixed respiratory alkalosis and metabolic acidosis
7
Q
Features of salicylate overdose
A
Hyperventilation
tinnitus
lethargy
sweating/pyrexia
nausea/vomiting
hyper and hypoglycaemia
seizures
coma
8
Q
Treatment for salicylate overdose
A
general (ABC, charcoal)
urinary alkalisation with IV sodium bicarbonate (enhances elimination of aspirin in the urine)
haemodialysis
9
Q
What is central diabetes insipidus treated with
A
desmopressin
10
Q
Causes of diabetes insipidus
A
idiopathic
post head injury
pituitary surgery
craniopharyngiomas
infiltrative
histiocytosis X
sarcoidosis
DIDMOAD is the association of cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness (also known as Wolfram’s syndrome)
haemochromatosis
11
Q
Causes of nephrogenic diabetes insipidus
A
genetic: the more common form affects the vasopression (ADH) receptor, the less common form results from a mutation in the gene that encodes the aquaporin 2 channel
electrolytes: hypercalcaemia, hypokalaemia
lithium
lithium desensitizes the kidney’s ability to respond to ADH in the collecting ducts
demeclocycline
tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis
12
Q
Investigation results for diabetes insipidus
A
high plasma osmolality, low urine osmolality
a urine osmolality of >700 mOsm/kg excludes diabetes insipidus
water deprivation test
13
Q
Management of diabetes insipidus
A
Nephrogenic DI: thiazides, low salt/protein diet
Central DI: treated with desmopressin
14
Q
Adrenal cortex mnemonic
A
GFR - ACD
zona Glomerulosa (on outside) - mineralocorticoids , mainly Aldosterone
zona Fasciculata (middle) - glucocorticoids, mainly Cortisol
zona Reticularis (on induise) - androgens, mainly Dehydroepiandrosterone (DHEA)
15
Q
What is Renin
A
an enzyme that is released by the renal juxtaglomerular cells in response to reduced renal perfusion
other factors that stimulate renin secretion include hyponatraemia, sympathetic nerve stimulation
hydrolyses angiotensinogen to form angiotensin I
16
Q
What is angiotensin II
A
angiotensin-converting enzyme (ACE) in the lungs converts angiotensin I → angiotensin II
angiotensin II has a wide variety of actions:
causes vasoconstriction of vascular smooth muscle leading to raised blood pressure and vasoconstriction of efferent arteriole of the glomerulus → increased filtration fraction (FF) to preserve GFR. Remember that FF = GFR / renal plasma flow
stimulates thirst (via the hypothalamus)
stimulates aldosterone and ADH release
increases proximal tubule Na+/H+ activity
17
Q
How to calculate anion gap
A
(sodium + potassium) - (bicarbonate + chloride)
18
Q
Causes of normal anion gap or hypercholeramic metabolic acidosis
A
GI bicarb loss: diarrhoea, ureterosigmoidostomy, fistula
Renal tubular acidosis
drugs: e.g. acetazolamide
Ammonium chloride injection
Addisons disease
19
Q
Causes of raised anion gap metabolic acidosis
A
lactate: shock, hypoxia
Ketones: DKA,alcohol
urate: renal failure
acid poisoning: salicylates, methanol
5-oxoproline: chronic paracetamol use
20
Q
If someone has chronic kidney disease what type of diet should you advise
A
A diet that is low in protein, phosphate, potassium and sodium
Because:
Protein - source of ammonia normally excreted by the kidney (but less so in CKD)
Phosphate - can complex with calcium to cause renal stones
Sodium - increases BP which further damages the kidney
Potassium - not well excreted by failing kidneys and can cause cardiac arrhythmias
21
Q
What is IgA nephropathy also known as
A
Berger’s disease
22
Q
What is IgA nephropathy and how does it classically present
A
commonest cause of glomerulonephritis worldwide
classically presents as macroscopic haematuria in young people following an upper respiratory tract infection
23
Q
conditions associated with IgA nephropathy
A
Alcoholic cirrhosis
Coeliac disease/dermatitis herpetiformis
Henoch-schonlein purpura
24
Q
Pathophysiology of IgA nephorpathy
A
Thought to be caused by mesangial depositio of IgA immune complexes
Histology shows mesangial hypercellularity, positive immunofluorescence for IgA and C3
25
Typical presentation of IgA nephropathy
Young male, recurrent episodes of macroscopic haematuria
associated with recent respiratory tract infections
nephrotic range proteinuria is rare
Renal failure is unusual and seen in minority of patients
26
Differentiating between IgA nephropathy and post-streptococcal glomerulonephritis
post-streptococcal glomerulonephritis associated with low complement levels
Main symptom in post-streptococcal glomerulonephritis is proteinuria
typically interval between URTI and onset of renal problems in post-streptococcal glomerulonephritis (In IgA its straight after)
27
\Management for IgA nephropathy
Isolated hematuria, no or minimal proteinuria and normal GFR then no treatment needed, follow up to check renal function
persistent proteinuria (>500-1000mg/day), with a normal or slightly reduced GFR then initial treatment with ACE inhibitprs
Active disease (failing GFR) or failure to respond to ACE inhibitors then immunosuppresion with corticosteroids
28
Prognosis in IgA nephropathy
Good prognosis markers = frank haematuria
Poor prognosis markers = male gender, proteinuria (especially >2g/day), HTN, smoking, hyperlipidaemia, ACE genotype DD
29
How does metoprolol work (especially in the renal function)
Beta blocker
Reduces blood pressure by reducing heart rate and cardiac output
Renal system:
blocks beta 1 adrenergic receptors in juxtaglomerular apparatus in the kidneys leading to a decrease in renin secretion
Renin converts angiotensin to angiotensin I which is then further converted to angiotensin II by ACE secreted from the lungs
Angiotensin II increases BP by vasocontriction and sodium retention
Therefore by directly blocking the release of renin, metoprolol causes a fall in blood pressure
30
what conditions is palmar xanthoma seen
Remnant hyperlipidaemia
May less commonly be seen in familial hypercholesterolaemia
31
What is eruptive xanthoma and what is it seen in
due to high triglyceride levels and present as multiple red/yellow vesicles on extensor surfaces
Causes:
Familial hypertriglyceridaemia
Lipoprotein lipase deficiency
32
What conditions is tendon xanthoma, tuberous xanthoma and xanthalesma seen in
familial hypercholesterolaemia
remnant hyperlipidaemia
33
Relationships of the right adrenal gland
diaphragm - posteriorly
kidney - inferiorly
vena cava - medially
hepatorenal pouch and bare area of the liver - anteriorly
34
Relationships of the left adrenal gland
Crus of the diaphragm - potero medially
pancreas and splenic vessels - inferiorly
lesser sac and stomach - anteriorly
35
Arterial supply of adrenal glands
Superior adrenal arteries - from inferior phrenic artery
Middle adrenal arteries - from aorta
Inferior adrenal arteries - from renal arteries
36
Venus drainage of right and left adrenal glands
right = via one central vein directly into IVC
Left = via one central vein into left renal vein
37
passage of blood to a nephron
afferent arteriole - glomerular capillary bed - efferent arteriole - peritubular capillaries and medullary vasa recta
38
GFR
total volume of plasma per unit time leaving the capillaries and entering the Bowmans capsule
39
Tubular function
reabsorption and secretion of substances occurs in tubules
Substances to be secreted into tubules are taken up from peritubular blood by tubular cells
40
When is glomerulosclerosis seen
in diabetic nephropathy but is not observed in minimal change disease
41
when is podocyte effacement seen
in minimal change disease on electron microscopy
42
When is spike and dome alterations seen
seen in membranous nephropathy which is a common cause of nephrotic syndrome in adults
43
When is thyroidisaton of the kidney seen
in the context of chronic pyelonephritis
44
What is minimal change disease
always presents as nephrotic syndrome (accounting for 75% of cases in children and 25% cases in adults)
Majority cases are idiopathic
45
Causes of minimal change disease
majority are idiopathic
in 10-20% cases:
Drugs: NSAIDS, rifampcin
Hodgkin's lymphoma, thymoma
Infectious mononucleosis
46
Pathophysiology of minimal change disease
T cell and cytokine mediated damage to the glomerular basement membrane - polyanion loss
resultant reduction of electrostatic charge - increased glomerular permeability to serum albumin
47
Features of minimal change disease
Nephrotic syndrome
normotension (hypertension is rare)
Highly selective proteinuria (only intermediate sized proteins such as albumin and transferrin leak through glomerulus)
Renal biopsy (normal glomeruli on light microscopy, electron microscopy shows fusion of podocytes and effacement of foot processes)
48
Management of minimal change disease
Oral corticosteroids (80% cases are responsive)
cyclophosphamide next step for steroid resistant cases
49
Causes of increased serum potassium
MACHINE
M- medications (ACE inhibitors, NSAIDS)
A - acidosis - metabolic and respiratory
C - cellular destruction (Burns, traumatic injury)
H - hypoaldosteronism, haemolysis
I - intake - excessive
N -Nephrons, renal failure
E - excretion - impaired
50
foods that are high in potassium
Salt substitutes
bananas, oranges, kiwi, avocado, spinach, tomatos
51
What is autosomal dominant polycystic kidney disease (and the two types)
most common inherited cause of kidney disease
ADPKD type 1 : 85% cases, affects chromosome 16, presents with renal failure earlier
ADPKD type 2 : 15% cases, affects chromosome 4
52
Ultrasound diagnostic criteria for ADPKD (in patients with a positive family history)
two cysts, unilateral or bilateral if aged <30
two cysts in both kidneys if aged 30-59
Four cysts in both kidneys if aged >60
53
Management of ADPKD
tolvaptan (vasopressin receptor 2 antagonist) may be an option. recommended if:
they have CKD stage 2 or 3 at the start of treatment
there is evidence of rapidly progressing disease
54
What is Alport's syndrome
X-dominant inherited
Due to a defect in the gene which codes for type IV collagen resulting in an abnormal glomerular basement membrane
disease is more severe in males with females rarely developing renal failure
55
Alport's syndrome features
Usually presents in childhood
presents with:
microscopic haematuria
progressive renal failure
bilateral sensoineural deafness
lenticonus: protrusion of the lens surface into the anterior chamber
retinitis pigmentosa
renal biopsy: splitting of lamina densa seen on electron microscopy
56
How to diagnose alport's syndrome
molecular genetic testing
renal biopsy: electron microscopy- longitudinal splitting of the lamina densa on the glomerular basement membrane resulting in a basket weave appearance
57
Where does the majority of renal phosphate reabsorption occure
in the proximal convoluted tubule
58
Localised prostate cancer (T1/T2) treatment
conservative: active monitoring and watchful wiating
radical prostatectomy
radiotherapy: external beam and brachytherapy
59
What IV therapy should you NOT use in a patient with hyperkalaemia
Hartmans - contains potassium
60
If large volumes of 0.9% saline is given to a patient what could happen
they could develop hyperchloraemic metabolic acidosis
61
what type of cancer is 90% of bladder cancer cases
transitional cell carcinoma
62
what type of cancer is 90% of bladder cancer cases
transitional cell carcinoma
63
Relationship between NSAIDs and the kidneys
NSAIDs (anti-inflammatory drug) inhibit the enzymes COX-1 and COX-2
these enzymes are responsible for the synthesis of prostaglandins
In the kidneys prostaglandins cause vasodilation of the afferent arterioles of the glomeruli (allowing for a higher rate of blood flow into the glomerulus and increase in GFR)
64
Pre renal causes of AKI
Ischaemia of lack of blood flow to the kidneys
examples: hypovolaemia secondary to diarrhoea/vomiting
renal artery stenosis
65
Intrinsic causes of AKI
damage to glomeruli, renal tubules or interstitium of the kidneys
Examples:
glomerulonephritis
acute tubular necrosis (ATN)
acute interstitial nephritis (AIN)
rhabdomyolysis
tumour lysis syndrome
66
Post renal causes of AKI
obstruction to the urine coming from the kidneys resulting in things backing up
Examples:
kidney stone in ureter or bladder
benign prostatic hyperplasia
external compression of the ureter
67
Risk factors for AKI
CKD
organ failure/chronic disease: heart failure, liver disease, DM
history of AKI
use of nephrotoxic drugs (NSAIDs, aminoglycosides, ACE inhibitors, angiotensin II receptor antagonists and diuretics)
Use of iodinated contrast agents within the past week
>65years of age
68
How to identify AKI
reduced urine output (oliguria = <0.5ml/kg/hour)
fluid overload
rise in molecules the kidneys usually excrete: potassium, urea and creatinine
69
symptoms/signs of AKI
reduced urine output
pulmonary and peripheral oedema
arrhythmias (secondary to changes in potassium and acid-base balance)
features of uraemia (pericarditis or encephalopathy)
70
Detection of AKI
U&Es
urinalysis
U/S if no identifiable cause for deterioration (within 24 hrs)
71
Management of AKI
management is largely supportive
require careful fluid balance to ensure kidneys are perfused but not overloaded
72
What drugs should be stopped in a patient with an AKI
NSAIDs (except if aspirin at cardiac dose, e.g. 75mg od)
Aminoglycosides
ACE inhibitors
Angiotensin II receptor antagonists
Diuretics
73
Who does haemolytic uraemic syndrome present in and what does it present with
generally seen in young children and produces a triad of:
AKI
microangiopathic haemolytic anaemia
thrombocytopenia
74
secondary causes of haemolytic uraemic syndrome (HUS)
most common cause is secondary
E.coli
Pneumoccocal infection
HIV
rare: SLE, drugs, cancer
75
Investigations for haemolytic uraemic syndrome
FBC: shows anaemia, thrombocytopenia and fragmented blood film
U&E: shows AKI
stool culture: look for evidence of STEC (E.coli)infection, PCR for shiga toxins
76
Management for haemolytic uraemic syndrome
supportive: fluids, blood transfusions and dialysis if required
77
Key features of seminoma
Commonest subtype of testicular cancer
average age of diagnosis is 40
78
Pathology of seminoma
sheet like lobular patterns of cells with substantial fibrous component
fibrous septa contain lymphocytic inclusions and granulomas may be seen
79
Risk factors for testicular cancer
cryptochidism
infertility
FH
Klinefelter's syndrome
Mumpss orchitis
80
Features of testicular cancer
painless lump
(pain can be present in a minority of cases)
Hydrocele, gynaecomastia
81
Diagnosis of testicular cancer
U/S is first line
Ct scan of chest/abdomen and pelvis for staging
tumour markers should be measured
82
Management of testicular cancer
orchidectomy (inguinal approach)
chemotherapy and radiotherapy depending on the staging
abdominal lesions >1cm following chemotherapy may require retroperitoneal lymph node dissection
83
Brief summary of epididymo-orchitis
acute epididymitis is acute inflammation of the epipidymis (often involving the testis and usually causes by bacterial infection)
>spreads from the urethra or bladder, in men <35 years gonorrhoea or chlamydia are the usual infections
>amiodarone is a non-infective cause, resolves on stopping the drug
>tenderness is confined to the epididymis
84
communicating hydrocele
accumulation of fluid within the tunica vaginalis
caused by patency of the processus vaginalis allowing peritoneal fluid to drain down into the scrotum. Communicating hydroceles are common in newborn males (clinically apparent in 5-10%) and usually resolve within the first few months of life
85
non-communicating hydrocele
caused by excessive fluid production within the tunica vaginalis
86
Features of hydrocele
soft, non-tender swelling of the hemi-scrotum (usually anterior and below the testicle)
Swelling is confined to the scrotum, you can get above the mass on examination
transilluminate with a pen tourch]
testis may be difficult to palpate if the hydrocele is large
87
Management of hydrocele
infantile hydroceles are generally repaired if they do not resolve spontaneously by the age of 1-2
in adults a conservative approach may be taken depending on the severity of the presentation
88
At what systolic pressures are the kidneys able to autoregulate their blood flow
80-180mmHg
89
Where do loop diuretics (like frusemide) act
what carrier or channel is inhibted
what is the percentage of filtered sodium excreted
ascending loop of henle
Na+/K+ 2Cl- carrier
up to 25%
90
Where do loop diuretics (like frusemide) act
what carrier or channel is inhibited
what is the percentage of filtered sodium excreted
Ascending limb of loop of henle
Na+/K+ 2Cl - carrier
up to 25%
91
Where do thiazide diuretics act
what carrier or channel is inhibited
what is the percentage of filtered sodium excreted
distal tubule and connecting segment
na+cl- carrier
between 3-5%
92
Where do K+ sparing diuretics (like spironolactone) act
what carrier or channel is inhibited
what is the percentage of filtered sodium excreted
cortical collecting tubule
Na+/K+ ATP ase pump
between 1-2%
93
SIADH generic causes (syndrome of inappropriate ADH secretion
malignancy
neurological
infections
drugs
other causes (PEEP, prophyrias)
94
Malignant causes of SIADH
small cell lung cancer (most commonly)
pancreas
prostrate
95
Neurological causes of SIADH
stroke
subarachnoid haemorrhage
subdural haemorrhage]
meningitis/encephalitis/abscess
96
Infection causes of SIADH
tuberculosis
pneumonia
97
Drug causes of SIADH
sulfonylureas
SSRIs, tricyclics
carbamazepine
vincristine
cyclophosphamide
98
Management of SIADH
correction must be done slowly to avoid precipitating central pontine myelinolysis
fluid restriction
declocycline: reduces responsiveness of collecting tubule to ADH
ADH (vasopressin) receptor antagonists have been developed
99
calcium oxalate stone
hypercalciuria is a major risk factor
hperoxaluria can increase risk
hypocitraturia increases risk because citrate forms complexes with calcium making it more soluble
stones are radio-opaque (less so than calcium phosphate stones0
hyperuricosuria may cause uric acid stones to which calcium oxalate binds
100
what infection is most likely to cause staghorn calculi
proteus mirabilis
has a urease producing enzyme
tends to favour urinary alkalinisation which is a relative prerequisite for forming staghorn calculi
101
what is anti-glomerular basement membrane )GBM) disease (AKA goodpasture's syndrome)
rare type of small-vessel vasculitis associated with pulmonary haemorrhage and rapidly progressive glomerulonephritis
caused by anti-GBM antibodies against type IV collagen
more common in men and has a bimodal age distribution (peaks in 20-30 and 60-70)
Associated with HLA DR2
102
features of anti-glomerular basement membrane disease (goodpasture's syndrome)
pullmonary haemorrhage
rapidly progressive glomerulonephritis (typically rapid onset AKI, nephritis -> proteinuria +haematuria)
103
Investigations for anti-glomerular basement membrane disease (goodpasture's syndrome)
renal biopsy: linear IgG deposits along the basement membrane
raised transfer factor secondary to pulmonary haemorrhages
104
management of anti-glomerular basement membrane disease (goodpasture's syndrome)
plasma exchange
steroids
clycophosphamide
105
Factors that increase the likelihood of a pulmonary haemorrhage in anti-glomerular basement membrane disease (goodpasture's syndrome)
smoking
LRTI
pulmonary oedema
inhalation of hydrocarbons
young males
106
What is aldosterone
released by the zona glomerulosa in response to raised angiotensin II, potassium, and ACTH levels
causes retention of Na+ in exchange for K+/H+ in distal tubule
107
Arterial supply for bladder
superior and inferior vesicle arteries (branches of internal iliac artery)
108
Venous drainage of the bladder
males = vesicoprostatic venous plexus
females = vesicouterine venous plexus
109
Lymphatic drainage of the bladder
external iliac nodes and internal iliac nodes
110
Histology of membranous glomerulonephritis
basement thickening on light microscopy
sub epithelial spikes on silver stain
positive immunohistochemistry for PLA2
111
Brief description of membranous glomerulonephritis
commonest type of glomerulonephritis in adults and third most common cause of end stage renal failure (ESRF)
usually presents with nephrotic syndrome or proteinuria
112
Causes of membranous glomerulonephritis
idiopathic = due to anti-phospholipase A2 antibodies
infections = hep b, malaria, syphilis
malignancy = prostate, lung, lymphoma, leukaemia
drugs = gold, penicillamine, NSAIDs
autoimmune disease = SLE, thyroiditis, rheumatoid
113
Management of membranous glomerulonephritis
all patients should receive an ACE inhibitor or an ARB
(reduce proteinuria/improve prognosis)
immunosuppression (only in severe cases, most resolve spontaneously)
consider anticoagulation for high risk patients
114
Prognosis for membranous glomerulonephritis
rule of thirds
one third - spontaneous remission
one third - remain proteinuria
one third - develop ESRF
115
Nephrotic syndrome triad
proteinuria >3g/24hr causing
hypoalbuminaemia (<30g/L) and
oedema
116
complications of nephrotic syndrome
increased risk of thromboembolism (related to loss of antithrombin III) and plasminogen in the urine
hyperlipidaemia (increased risk of ACS)
CKD
Increased risk of infection due to loss of immunoglobulins in urine
hypocalcaemia vit D and binding protein lost in urine)
117
haematochezia
passage of fresh blood through anus
118
What is ischamic colitis
acute but transient compromise to the blood flow to the large bowel
can lead to inflammation, ulceration and haemorrhage
more likely at splenic flexure (because it is closely situated to the SMA and IMA)
thumb printing may be seen on abdominal Xray due to mucosal oedema/haemorrhage
119
Acute mesenteric embolus
most common cause of mesenteric vessel disease
sudden onset abdo pain followed by profuse diarrhoea
may be associated with vomiting
rapid clinical deterioration
WCC, lactate, amylase may be abnormal in established disease
120
Mesenteric vein thrombosis
usually a history over a week
Overt abdominal signs and symptoms will not occur until venous thrombosis has reached a stage to compromise arterial inflow.
Thrombophilia accounts for 60% of cases.
121
Management of mesenteric vessel disease
Overt signs of peritonism: Laparotomy
Mesenteric vein thrombosis: If no peritonism: Medical management with IV heparin
At operation limited resection of frankly necrotic bowel with view to relook laparotomy at 24-48h. In the interim urgent bowel revascularisation via endovascular (preferred) or surgery.
122
Where does the bladder receive parasympathetic innveration
pelvic splanchnic nerves
123
Acute bacterial prostitis
Acute bacterial prostatitis is typically caused by gram-negative bacteria entering the prostate gland via the urethra.
Escherichia coli is the most commonly isolated pathogen.
124
Risk factors for acute bacterial prostitis
Risk factors for acute bacterial prostatitis include recent urinary tract infection, urogenital instrumentation, intermittent bladder catheterisation and recent prostate biopsy.
125
Features of acute bacterial prostitis
the pain of prostatitis may be referred to a variety of areas including the perineum, penis, rectum or back
obstructive voiding symptoms may be present
fever and rigors may be present
digital rectal examination: tender, boggy prostate gland
126
Management of acute bacterial prostitis
Clinical Knowledge Summaries currently recommend a 14-day course of a quinolone
consider screening for sexually transmitted infections
127
Where does majority of glucose reabsorption in the nephron occur
within the proximal convoluted tubule
128
What reaction does renin catalyse
, catalysing a hydrolysis reaction that converts angiotensinogen into angiotensin I.
129
What is frothy urine
a sign of proteinuria
130
Nephritic syndrome
describes the presentation of disease which causes protein and blood to be present in the urine. Patients with nephritic syndrome typically present with haematuria, oliguria, and hypertension.
131
Nephrotic vs nephritic syndrome
nephrotic = proteinuria and oedema
Nephritic = haematuria and hypertension
132
definitive treatment of choice for a child with posterior urethral valves
endoscopic valvotomy
133
erysipelas
a bacterial skin infection involving the upper dermis that characteristically extends into the superficial cutaneous lymphatics. It is a tender, intensely erythematous, indurated plaque with a sharply demarcated border
134
How does penicillin cause AKI
by causing acute interstitial nephritis
135
Drugs that cause acute interstital nephritis
penicillin
rifampicin
NSAIDs
allopurinol
furosemide
136
Pathophysiology of acute interstitial nephritis
histology: marked interstitial oedema and interstitial infiltrate in the connective tissue between renal tubules
137
Features of acute interstitial nephritis
fever, rash, arthralgia
eosinophilia
mild renal impairment
hypertension
138
Investigations for acute interstitial nephirits
sterile pyuria
white cell casts
139
Tubulointerstital nephritis with uveitis
Tubulointerstitial nephritis with uveitis (TINU) usually occurs in young females. Symptoms include fever, weight loss and painful, red eyes. Urinalysis is positive for leukocytes and protein.
140
What is Hyperacute transplant rejection caused by
caused by pre-existing antibodies against ABO or HLA antigens
. If widespread, this can lead to activation of the coagulation cascade and eventual occlusive thrombosis of the donated organ.
141
What is spironalctone
an aldosterone antagonist which acts in the cortical collecting duct.
potassium sparing diuretic
142
Indications for spironolactone
ascites: patients with cirrhosis develop a secondary hyperaldosteronism. Relatively large doses such as 100 or 200mg are often used
hypertension: used in some patients as a NICE 'step 4' treatment
heart failure (see RALES study below)
nephrotic syndrome
Conn's syndrome
143
Adverse effects of spironoalctone
hyperkalaemia
gynaecomastia: less common with eplerenone
144
Classes of blood loss in ml
Class I <750ml
Class II 750-1500ml
Class III 1500-2000ml
Class IV >2000ml
145
What epithelia is the bladder lined with
transitional epithelium
146
What is characteristic of lupus nephritis
Proliferative 'wire-loop' glomerular histology in the presence of proteinuria and systemic symptoms
147
WHO classifications of renal complications of systemic lupus erythematosus
class I: normal kidney
class II: mesangial glomerulonephritis
class III: focal (and segmental) proliferative glomerulonephritis
class IV: diffuse proliferative glomerulonephritis
class V: diffuse membranous glomerulonephritis
class VI: sclerosing glomerulonephritis
148
Management of renal complications of systemic lupus erythematosus
treat hypertension
initial therapy for focal (class III) or diffuse (class IV) lupus nephritis
glucocorticoids with either mycophenolate or cyclophosphamide
subsequent therapy
mycophenolate is generally preferred to azathioprine to decrease the risk of developing end-stage renal disease
149
Site of action of frusemide
ascending limb of the loop of Henle
150
What is the difference in the physiological compensatory mechanism for a venous bleed compared with an arterial bleed in the short-term?
a venous bleed is compensated in a less direct way. Firstly, a venous bleed reduces preload, which reduces cardiac output and therefore blood pressure. This reduction in blood pressure is detected by baroreceptors, which signal a physiological compensation.
151
Loss of which enzyme causes steatorrhoea
Lipase
152
Drugs that should be stopped in AKI
NSAIDS (except aspirin at cardiac dose)
aminoglycosides
ACE inhibitors
Angiotensin II receptor antagonists
Diuretics
153
How to short term shift in potassium from ECF to ICF
combined insulin/dextrose infusion
nebulised salbutamol
154
Drugs to remove potassium from body
calcium resonium (orally or enema)
loop diuretic
dialysis
155
Henoch schonlein purpura
IgA mediated small vessel vasculitis
usually seen in children following an infection
156
Features of henoch schonlein purpura
and treatment
palpable purpuric rash (with localised oedema) over buttocks and extensor surfaces of arms and legs
abdominal pain
polyarthritis
features of IgA nephropathy may occur
treatment = analgesia for arthralgia, treatment of nephropathy is generally supportive
157
Urine in acute tubular necrosis
brown granular casts in urine
158
What is it if you see red cell casts in the urine
nephritic syndrome
159
Differences between IgA nephropathy and post-streptococcal glomerulonephritis
IgA nephropathy = develops 1-2 days after URTI, young males, macroscopic haematuria
Post-streptococcal glomerulonephritis = develops 1-2 weeks after URTI, proteinuria, low complement
SIMILARITIES = recent URTI and haematuria
160
Disequilibrium syndrome (DDS)
is a rare but serious complication of hemodialysis. It is characterized mainly by neurological symptoms such as fatigue, mild headaches, nausea, vomiting, disturbed consciousness, convulsions and coma. The symptoms are usually mild, transient and self-limiting and rarely, it can be fatal.
161
Features of testicular torsion
Pain is usually severe and of sudden onset
pain may be referred to lower abdomen
N + V
on examination - swollen, tender testis retracted upwards, skin may be reddened
cremasteric reflex is lost
elevation of testis does not ease the pain (Prehn's sign)
162
Management of testicular torsion
urgent surgical exploration
if a torted testis is identified then both testis should be fixed as the condition of bell clapper testis is often bilateral
163
voiding symptoms (urology) management
conservative measures include: pelvic floor muscle training, bladder training, prudent fluid intake and containment products
if moderate/severe offer alpha blocker
if prostate is enlarged offer 5-alpha reductase inhibitor
164
Overactive bladder management
conservative measures include moderating fluid intake
bladder retraining should be offered
anti-muscarinic drugs should be offered if symptoms persist - NICE recommend oxybutynin (immediate release), tolterodine (immediate release) or darifenacin (once daily preparation)
mirabegron may be considered if first line drugs fail
165
Nocturia management
advise about moderating flui intake at night
furosemide 40mg late afternoon may be considered
desmopressin may be helpful
166
Renal colic what analgesia do you give
IM Diclofenac
167
Symptom triad in renal cell carcinoma
haematuria
flank pain
palpable mass
168
Risk factors for developing renal cell carcinoma
End stage renal failure
smoking
obesity
HTN
tubular sclerosis
169
Where does renal cell carcinoma spread to? (classic presentation)
Cannonball metastases in the lungs
often spreads to renal vein then IVC
To tissues around kidney -> within Gerota's fascia
170
Paraneoplastic features of renal cell carcinoma
polycythaemia (due to secretion of unregulated erythropoietin)
hypercalcaemia
HTN
171
Surgical management of renal cell carcinoma
partial nephrectomy
radical nephrectomy
172
What is haemachromotosis
iron storage disorder that results in excessive total body iron and deposition of iron in tissues
autosomal recessive
173
Symptoms of haemochromatosis
Bronze discolouration
chronic fatigue
Hair loss
erectile dysfunction
cognitive dysfunction
joint pain
presents over age of 40
174
How to make a diagnosis of haemochromotosis
Serum ferritin level (high - because it is an acute phase reactant)
Transferrin level (high - helpful in distinguishing between high ferritin from iron overload or from NAFLD)
Liver biopsy with Perl's stain
Genetic testing (C282Y and H63D mutations)
CT abdo - increase attenuation of the liver
MRI - can show iron deposits in heart
175
Complications of haemochromatosis
T1DM
Liver cirrhosis
Reversible cardiomyopathy
hepatocellular carcinoma
Hypothyroidism
176
First and second line management of haemachromatosis
Venesection - first line
Desferrioxamine (Second line)
Monitor serum ferritin
Avoid alcohol
Genetic counselling
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NICE criteria for AKI
- Rise in creatinine of >25micromol/L in 48hrs
- Rise in creatinine >50% in 7 days
- Urine output <0.5ml/kg/hour for >6hrs
178
Risk factors for AKI
CKD
heart failure
Diabetes
>65
Nephrotoxic drugs - NSAIDs, ACE inhibitors
use of contrast - CT
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Pre renal causes for AKI
due to inadequate blood supply to kidneys:
Dehydration
hypotension
Heart failure
180
Renal causes of AKI
Where intrinsic kidney disease is leading to reduced filtration of the blood
Glomerulonephritis
Interstitial nephritis
acute tubular necrosis
181
Post renal causes of AKI
Caused by obstruction of urine from the kidneys, causing back pressure and reduced kidney function
Urinary tract calculi
Masses (cancer)
Ureter or urethral strictures
Enlarged prostate or prostate cancer
182
Investigations for AKI
Urinalysis for blood, protein, leukocytes, nitrites and glucose
US for obstruction
U&Es
183
Management of AKI
CORRECT THE UNDERLYING CAUSE:
- Fluid rehydration in patients with pre-renal cause
- Stop nephrotoxic medications such as NSAIDs and antihypertensives that reduce the filtration pressure (i.e. ACE inhibitors → ramipril)
- Relieve obstruction in post renal AKI, for example inset a catheter for a patient in retention with an enlarged prostat
184
What is nephrotic syndrome
occurs when basement membrane in glomerulus becomes highly permeable to protein - allows protein to leak from the blood into the urine
185
Triad of symptoms for nephrotic syndrome
Low serum albumin
High urine protein content
Oedema
186
Causes of nephrotic syndrome
children - minimal change disease
intrinsic kidney disease such as:
focal segmental glomerulonephritis
membranoproliferative glomerulonephritis
secondary to underlying systemic illness:
HSP
Diabetes
infection - such as HIV, hepatitis, malaria
187
Minimal change disease
Renal biopsy
