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Year 3 > Urology and renal > Flashcards

Urology and renal Flashcards

1
Q

what is Lymphogranuloma venereum (LGV) caused by

A

Chlamydia trachomatis serovars L1, L2 and L3

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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

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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

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4
Q

How is Lymphogranuloma venereum (LGV) treated

A

doxycycline

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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

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6
Q

Key concept for Salicylate overdose

A

leads to mixed respiratory alkalosis and metabolic acidosis

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7
Q

Features of salicylate overdose

A

Hyperventilation
tinnitus
lethargy
sweating/pyrexia
nausea/vomiting
hyper and hypoglycaemia
seizures
coma

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8
Q

Treatment for salicylate overdose

A

general (ABC, charcoal)
urinary alkalisation with IV sodium bicarbonate (enhances elimination of aspirin in the urine)
haemodialysis

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9
Q

What is central diabetes insipidus treated with

A

desmopressin

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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

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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

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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

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13
Q

Management of diabetes insipidus

A

Nephrogenic DI: thiazides, low salt/protein diet
Central DI: treated with desmopressin

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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)

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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

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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

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17
Q

How to calculate anion gap

A

(sodium + potassium) - (bicarbonate + chloride)

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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

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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

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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

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21
Q

What is IgA nephropathy also known as

A

Berger’s disease

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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

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23
Q

conditions associated with IgA nephropathy

A

Alcoholic cirrhosis
Coeliac disease/dermatitis herpetiformis
Henoch-schonlein purpura

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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

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25
Q

Typical presentation of IgA nephropathy

A

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

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26
Q

Differentiating between IgA nephropathy and post-streptococcal glomerulonephritis

A

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)

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27
Q

\Management for IgA nephropathy

A

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

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28
Q

Prognosis in IgA nephropathy

A

Good prognosis markers = frank haematuria
Poor prognosis markers = male gender, proteinuria (especially >2g/day), HTN, smoking, hyperlipidaemia, ACE genotype DD

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29
Q

How does metoprolol work (especially in the renal function)

A

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

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30
Q

what conditions is palmar xanthoma seen

A

Remnant hyperlipidaemia
May less commonly be seen in familial hypercholesterolaemia

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31
Q

What is eruptive xanthoma and what is it seen in

A

due to high triglyceride levels and present as multiple red/yellow vesicles on extensor surfaces
Causes:
Familial hypertriglyceridaemia
Lipoprotein lipase deficiency

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32
Q

What conditions is tendon xanthoma, tuberous xanthoma and xanthalesma seen in

A

familial hypercholesterolaemia
remnant hyperlipidaemia

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33
Q

Relationships of the right adrenal gland

A

diaphragm - posteriorly
kidney - inferiorly
vena cava - medially
hepatorenal pouch and bare area of the liver - anteriorly

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34
Q

Relationships of the left adrenal gland

A

Crus of the diaphragm - potero medially
pancreas and splenic vessels - inferiorly
lesser sac and stomach - anteriorly

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35
Q

Arterial supply of adrenal glands

A

Superior adrenal arteries - from inferior phrenic artery

Middle adrenal arteries - from aorta
Inferior adrenal arteries - from renal arteries

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36
Q

Venus drainage of right and left adrenal glands

A

right = via one central vein directly into IVC
Left = via one central vein into left renal vein

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37
Q

passage of blood to a nephron

A

afferent arteriole - glomerular capillary bed - efferent arteriole - peritubular capillaries and medullary vasa recta

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38
Q

GFR

A

total volume of plasma per unit time leaving the capillaries and entering the Bowmans capsule

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39
Q

Tubular function

A

reabsorption and secretion of substances occurs in tubules
Substances to be secreted into tubules are taken up from peritubular blood by tubular cells

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40
Q

When is glomerulosclerosis seen

A

in diabetic nephropathy but is not observed in minimal change disease

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41
Q

when is podocyte effacement seen

A

in minimal change disease on electron microscopy

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42
Q

When is spike and dome alterations seen

A

seen in membranous nephropathy which is a common cause of nephrotic syndrome in adults

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43
Q

When is thyroidisaton of the kidney seen

A

in the context of chronic pyelonephritis

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44
Q

What is minimal change disease

A

always presents as nephrotic syndrome (accounting for 75% of cases in children and 25% cases in adults)
Majority cases are idiopathic

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45
Q

Causes of minimal change disease

A

majority are idiopathic
in 10-20% cases:
Drugs: NSAIDS, rifampcin
Hodgkin’s lymphoma, thymoma
Infectious mononucleosis

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46
Q

Pathophysiology of minimal change disease

A

T cell and cytokine mediated damage to the glomerular basement membrane - polyanion loss
resultant reduction of electrostatic charge - increased glomerular permeability to serum albumin

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47
Q

Features of minimal change disease

A

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)

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48
Q

Management of minimal change disease

A

Oral corticosteroids (80% cases are responsive)
cyclophosphamide next step for steroid resistant cases

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49
Q

Causes of increased serum potassium

A

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

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50
Q

foods that are high in potassium

A

Salt substitutes
bananas, oranges, kiwi, avocado, spinach, tomatos

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51
Q

What is autosomal dominant polycystic kidney disease (and the two types)

A

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

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52
Q

Ultrasound diagnostic criteria for ADPKD (in patients with a positive family history)

A

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

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53
Q

Management of ADPKD

A

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

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54
Q

What is Alport’s syndrome

A

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

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55
Q

Alport’s syndrome features

A

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

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56
Q

How to diagnose alport’s syndrome

A

molecular genetic testing
renal biopsy: electron microscopy- longitudinal splitting of the lamina densa on the glomerular basement membrane resulting in a basket weave appearance

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57
Q

Where does the majority of renal phosphate reabsorption occure

A

in the proximal convoluted tubule

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58
Q

Localised prostate cancer (T1/T2) treatment

A

conservative: active monitoring and watchful wiating
radical prostatectomy
radiotherapy: external beam and brachytherapy

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59
Q

What IV therapy should you NOT use in a patient with hyperkalaemia

A

Hartmans - contains potassium

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60
Q

If large volumes of 0.9% saline is given to a patient what could happen

A

they could develop hyperchloraemic metabolic acidosis

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61
Q

what type of cancer is 90% of bladder cancer cases

A

transitional cell carcinoma

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62
Q

what type of cancer is 90% of bladder cancer cases

A

transitional cell carcinoma

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63
Q

Relationship between NSAIDs and the kidneys

A

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)

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64
Q

Pre renal causes of AKI

A

Ischaemia of lack of blood flow to the kidneys

examples: hypovolaemia secondary to diarrhoea/vomiting
renal artery stenosis

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65
Q

Intrinsic causes of AKI

A

damage to glomeruli, renal tubules or interstitium of the kidneys
Examples:
glomerulonephritis
acute tubular necrosis (ATN)
acute interstitial nephritis (AIN)
rhabdomyolysis
tumour lysis syndrome

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66
Q

Post renal causes of AKI

A

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

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67
Q

Risk factors for AKI

A

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

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68
Q

How to identify AKI

A

reduced urine output (oliguria = <0.5ml/kg/hour)
fluid overload
rise in molecules the kidneys usually excrete: potassium, urea and creatinine

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69
Q

symptoms/signs of AKI

A

reduced urine output
pulmonary and peripheral oedema
arrhythmias (secondary to changes in potassium and acid-base balance)
features of uraemia (pericarditis or encephalopathy)

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70
Q

Detection of AKI

A

U&Es
urinalysis
U/S if no identifiable cause for deterioration (within 24 hrs)

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71
Q

Management of AKI

A

management is largely supportive
require careful fluid balance to ensure kidneys are perfused but not overloaded

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72
Q

What drugs should be stopped in a patient with an AKI

A

NSAIDs (except if aspirin at cardiac dose, e.g. 75mg od)
Aminoglycosides
ACE inhibitors
Angiotensin II receptor antagonists
Diuretics

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73
Q

Who does haemolytic uraemic syndrome present in and what does it present with

A

generally seen in young children and produces a triad of:
AKI
microangiopathic haemolytic anaemia
thrombocytopenia

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74
Q

secondary causes of haemolytic uraemic syndrome (HUS)

A

most common cause is secondary
E.coli
Pneumoccocal infection
HIV
rare: SLE, drugs, cancer

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75
Q

Investigations for haemolytic uraemic syndrome

A

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
Q

Management for haemolytic uraemic syndrome

A

supportive: fluids, blood transfusions and dialysis if required

77
Q

Key features of seminoma

A

Commonest subtype of testicular cancer
average age of diagnosis is 40

78
Q

Pathology of seminoma

A

sheet like lobular patterns of cells with substantial fibrous component
fibrous septa contain lymphocytic inclusions and granulomas may be seen

79
Q

Risk factors for testicular cancer

A

cryptochidism
infertility
FH
Klinefelter’s syndrome
Mumpss orchitis

80
Q

Features of testicular cancer

A

painless lump
(pain can be present in a minority of cases)
Hydrocele, gynaecomastia

81
Q

Diagnosis of testicular cancer

A

U/S is first line
Ct scan of chest/abdomen and pelvis for staging
tumour markers should be measured

82
Q

Management of testicular cancer

A

orchidectomy (inguinal approach)
chemotherapy and radiotherapy depending on the staging
abdominal lesions >1cm following chemotherapy may require retroperitoneal lymph node dissection

83
Q

Brief summary of epididymo-orchitis

A

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
Q

communicating hydrocele

A

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
Q

non-communicating hydrocele

A

caused by excessive fluid production within the tunica vaginalis

86
Q

Features of hydrocele

A

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
Q

Management of hydrocele

A

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
Q

At what systolic pressures are the kidneys able to autoregulate their blood flow

A

80-180mmHg

89
Q

Where do loop diuretics (like frusemide) act
what carrier or channel is inhibted
what is the percentage of filtered sodium excreted

A

ascending loop of henle
Na+/K+ 2Cl- carrier
up to 25%

90
Q

Where do loop diuretics (like frusemide) act
what carrier or channel is inhibited
what is the percentage of filtered sodium excreted

A

Ascending limb of loop of henle
Na+/K+ 2Cl - carrier
up to 25%

91
Q

Where do thiazide diuretics act
what carrier or channel is inhibited
what is the percentage of filtered sodium excreted

A

distal tubule and connecting segment
na+cl- carrier
between 3-5%

92
Q

Where do K+ sparing diuretics (like spironolactone) act
what carrier or channel is inhibited
what is the percentage of filtered sodium excreted

A

cortical collecting tubule
Na+/K+ ATP ase pump
between 1-2%

93
Q

SIADH generic causes (syndrome of inappropriate ADH secretion

A

malignancy
neurological
infections
drugs
other causes (PEEP, prophyrias)

94
Q

Malignant causes of SIADH

A

small cell lung cancer (most commonly)
pancreas
prostrate

95
Q

Neurological causes of SIADH

A

stroke
subarachnoid haemorrhage
subdural haemorrhage]
meningitis/encephalitis/abscess

96
Q

Infection causes of SIADH

A

tuberculosis
pneumonia

97
Q

Drug causes of SIADH

A

sulfonylureas
SSRIs, tricyclics
carbamazepine
vincristine
cyclophosphamide

98
Q

Management of SIADH

A

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
Q

calcium oxalate stone

A

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
Q

what infection is most likely to cause staghorn calculi

A

proteus mirabilis
has a urease producing enzyme
tends to favour urinary alkalinisation which is a relative prerequisite for forming staghorn calculi

101
Q

what is anti-glomerular basement membrane )GBM) disease (AKA goodpasture’s syndrome)

A

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
Q

features of anti-glomerular basement membrane disease (goodpasture’s syndrome)

A

pullmonary haemorrhage
rapidly progressive glomerulonephritis (typically rapid onset AKI, nephritis -> proteinuria +haematuria)

103
Q

Investigations for anti-glomerular basement membrane disease (goodpasture’s syndrome)

A

renal biopsy: linear IgG deposits along the basement membrane
raised transfer factor secondary to pulmonary haemorrhages

104
Q

management of anti-glomerular basement membrane disease (goodpasture’s syndrome)

A

plasma exchange
steroids
clycophosphamide

105
Q

Factors that increase the likelihood of a pulmonary haemorrhage in anti-glomerular basement membrane disease (goodpasture’s syndrome)

A

smoking
LRTI
pulmonary oedema
inhalation of hydrocarbons
young males

106
Q

What is aldosterone

A

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
Q

Arterial supply for bladder

A

superior and inferior vesicle arteries (branches of internal iliac artery)

108
Q

Venous drainage of the bladder

A

males = vesicoprostatic venous plexus
females = vesicouterine venous plexus

109
Q

Lymphatic drainage of the bladder

A

external iliac nodes and internal iliac nodes

110
Q

Histology of membranous glomerulonephritis

A

basement thickening on light microscopy
sub epithelial spikes on silver stain
positive immunohistochemistry for PLA2

111
Q

Brief description of membranous glomerulonephritis

A

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
Q

Causes of membranous glomerulonephritis

A

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
Q

Management of membranous glomerulonephritis

A

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
Q

Prognosis for membranous glomerulonephritis

A

rule of thirds
one third - spontaneous remission
one third - remain proteinuria
one third - develop ESRF

115
Q

Nephrotic syndrome triad

A

proteinuria >3g/24hr causing
hypoalbuminaemia (<30g/L) and
oedema

116
Q

complications of nephrotic syndrome

A

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
Q

haematochezia

A

passage of fresh blood through anus

118
Q

What is ischamic colitis

A

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
Q

Acute mesenteric embolus

A

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
Q

Mesenteric vein thrombosis

A

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
Q

Management of mesenteric vessel disease

A

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
Q

Where does the bladder receive parasympathetic innveration

A

pelvic splanchnic nerves

123
Q

Acute bacterial prostitis

A

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
Q

Risk factors for acute bacterial prostitis

A

Risk factors for acute bacterial prostatitis include recent urinary tract infection, urogenital instrumentation, intermittent bladder catheterisation and recent prostate biopsy.

125
Q

Features of acute bacterial prostitis

A

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
Q

Management of acute bacterial prostitis

A

Clinical Knowledge Summaries currently recommend a 14-day course of a quinolone
consider screening for sexually transmitted infections

127
Q

Where does majority of glucose reabsorption in the nephron occur

A

within the proximal convoluted tubule

128
Q

What reaction does renin catalyse

A

, catalysing a hydrolysis reaction that converts angiotensinogen into angiotensin I.

129
Q

What is frothy urine

A

a sign of proteinuria

130
Q

Nephritic syndrome

A

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
Q

Nephrotic vs nephritic syndrome

A

nephrotic = proteinuria and oedema
Nephritic = haematuria and hypertension

132
Q

definitive treatment of choice for a child with posterior urethral valves

A

endoscopic valvotomy

133
Q

erysipelas

A

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
Q

How does penicillin cause AKI

A

by causing acute interstitial nephritis

135
Q

Drugs that cause acute interstital nephritis

A

penicillin
rifampicin
NSAIDs
allopurinol
furosemide

136
Q

Pathophysiology of acute interstitial nephritis

A

histology: marked interstitial oedema and interstitial infiltrate in the connective tissue between renal tubules

137
Q

Features of acute interstitial nephritis

A

fever, rash, arthralgia
eosinophilia
mild renal impairment
hypertension

138
Q

Investigations for acute interstitial nephirits

A

sterile pyuria
white cell casts

139
Q

Tubulointerstital nephritis with uveitis

A

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
Q

What is Hyperacute transplant rejection caused by

A

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
Q

What is spironalctone

A

an aldosterone antagonist which acts in the cortical collecting duct.
potassium sparing diuretic

142
Q

Indications for spironolactone

A

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
Q

Adverse effects of spironoalctone

A

hyperkalaemia
gynaecomastia: less common with eplerenone

144
Q

Classes of blood loss in ml

A

Class I <750ml
Class II 750-1500ml
Class III 1500-2000ml
Class IV >2000ml

145
Q

What epithelia is the bladder lined with

A

transitional epithelium

146
Q

What is characteristic of lupus nephritis

A

Proliferative ‘wire-loop’ glomerular histology in the presence of proteinuria and systemic symptoms

147
Q

WHO classifications of renal complications of systemic lupus erythematosus

A

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
Q

Management of renal complications of systemic lupus erythematosus

A

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
Q

Site of action of frusemide

A

ascending limb of the loop of Henle

150
Q

What is the difference in the physiological compensatory mechanism for a venous bleed compared with an arterial bleed in the short-term?

A

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
Q

Loss of which enzyme causes steatorrhoea

A

Lipase

152
Q

Drugs that should be stopped in AKI

A

NSAIDS (except aspirin at cardiac dose)
aminoglycosides
ACE inhibitors
Angiotensin II receptor antagonists
Diuretics

153
Q

How to short term shift in potassium from ECF to ICF

A

combined insulin/dextrose infusion
nebulised salbutamol

154
Q

Drugs to remove potassium from body

A

calcium resonium (orally or enema)
loop diuretic
dialysis

155
Q

Henoch schonlein purpura

A

IgA mediated small vessel vasculitis
usually seen in children following an infection

156
Q

Features of henoch schonlein purpura
and treatment

A

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
Q

Urine in acute tubular necrosis

A

brown granular casts in urine

158
Q

What is it if you see red cell casts in the urine

A

nephritic syndrome

159
Q

Differences between IgA nephropathy and post-streptococcal glomerulonephritis

A

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
Q

Disequilibrium syndrome (DDS)

A

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
Q

Features of testicular torsion

A

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
Q

Management of testicular torsion

A

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
Q

voiding symptoms (urology) management

A

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
Q

Overactive bladder management

A

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
Q

Nocturia management

A

advise about moderating flui intake at night

furosemide 40mg late afternoon may be considered

desmopressin may be helpful

166
Q

Renal colic what analgesia do you give

A

IM Diclofenac

167
Q

Symptom triad in renal cell carcinoma

A

haematuria
flank pain
palpable mass

168
Q

Risk factors for developing renal cell carcinoma

A

End stage renal failure
smoking
obesity
HTN
tubular sclerosis

169
Q

Where does renal cell carcinoma spread to? (classic presentation)

A

Cannonball metastases in the lungs
often spreads to renal vein then IVC
To tissues around kidney -> within Gerota’s fascia

170
Q

Paraneoplastic features of renal cell carcinoma

A

polycythaemia (due to secretion of unregulated erythropoietin)

hypercalcaemia

HTN

171
Q

Surgical management of renal cell carcinoma

A

partial nephrectomy
radical nephrectomy

172
Q

What is haemachromotosis

A

iron storage disorder that results in excessive total body iron and deposition of iron in tissues

autosomal recessive

173
Q

Symptoms of haemochromatosis

A

Bronze discolouration
chronic fatigue
Hair loss
erectile dysfunction
cognitive dysfunction
joint pain
presents over age of 40

174
Q

How to make a diagnosis of haemochromotosis

A

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
Q

Complications of haemochromatosis

A

T1DM
Liver cirrhosis
Reversible cardiomyopathy
hepatocellular carcinoma
Hypothyroidism

176
Q

First and second line management of haemachromatosis

A

Venesection - first line
Desferrioxamine (Second line)
Monitor serum ferritin
Avoid alcohol
Genetic counselling

177
Q

NICE criteria for AKI

A
  • Rise in creatinine of >25micromol/L in 48hrs
  • Rise in creatinine >50% in 7 days
  • Urine output <0.5ml/kg/hour for >6hrs
178
Q

Risk factors for AKI

A

CKD
heart failure
Diabetes
>65
Nephrotoxic drugs - NSAIDs, ACE inhibitors
use of contrast - CT

179
Q

Pre renal causes for AKI

A

due to inadequate blood supply to kidneys:
Dehydration
hypotension
Heart failure

180
Q

Renal causes of AKI

A

Where intrinsic kidney disease is leading to reduced filtration of the blood
Glomerulonephritis
Interstitial nephritis
acute tubular necrosis

181
Q

Post renal causes of AKI

A

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
Q

Investigations for AKI

A

Urinalysis for blood, protein, leukocytes, nitrites and glucose
US for obstruction
U&Es

183
Q

Management of AKI

A

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
Q

What is nephrotic syndrome

A

occurs when basement membrane in glomerulus becomes highly permeable to protein - allows protein to leak from the blood into the urine

185
Q

Triad of symptoms for nephrotic syndrome

A

Low serum albumin
High urine protein content
Oedema

186
Q

Causes of nephrotic syndrome

A

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
Q

Minimal change disease

A

Renal biopsy

Year 3 (14 decks)

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